Thermogenesis and body heat generation

Bpdy could also beat from a Protein for weight loss in athletes Thermogenesis and body heat generation depolarization that allows warm-sensitive neurons Thermogenesis and body heat generation reach their discharge threshold potential and then determines their discharge frequency Kobayashi et al. Advances in Physiology Education. Altered thermal selection behavior in mice lacking transient receptor potential vanilloid 4. All rights reserved. Thermogenic responses in brown-fat cells are fully UCP1-dependent: UCP2 or UCP3 do not substitute for UCP1 in adrenergically or fatty-acid induced thermogenesis.

Thermogenesis and body heat generation -
Cannon, B. Brown adipose tissue: Function and physiological significance. Roesler, A. UCP1-independent thermogenesis. Rosen, E. Adipocytes as regulators of energy balance and glucose homeostasis. Nature , , — Park, H. Lipid Regulators of Thermogenic Fat Activation.

Trends Endocrinol. TEM , 30, — Lynes, M. Lipokines and Thermogenesis. Endocrinology , , — Wikstrom, J. Hormone-induced mitochondrial fission is utilized by brown adipocytes as an amplification pathway for energy expenditure. Embo J. Bartelt, A. Brown adipose tissue activity controls triglyceride clearance.

Global Analysis of Plasma Lipids Identifies Liver-Derived Acylcarnitines as a Fuel Source for Brown Fat Thermogenesis. Cold-Activated Lipid Dynamics in Adipose Tissue Highlights a Role for Cardiolipin in Thermogenic Metabolism.

Cell Rep. Chaurasia, B. Adipocyte Ceramides Regulate Subcutaneous Adipose Browning, Inflammation, and Metabolism. Gohlke, S. Identification of functional lipid metabolism biomarkers of brown adipose tissue aging.

Leiria, L. Ceramides are necessary and sufficient for diet-induced impairment of thermogenic adipocytes. Hoene, M. The lipid profile of brown adipose tissue is sex-specific in mice. Acta , , — Justo, R. Brown adipose tissue mitochondrial subpopulations show different morphological and thermogenic characteristics.

Mitochondrion , 5, 45— Tajima, K. Mitochondrial lipoylation integrates age-associated decline in brown fat thermogenesis. Berry, D. Mouse strains to study cold-inducible beige progenitors and beige adipocyte formation and function.

Chen, Y. Thermal stress induces glycolytic beige fat formation via a myogenic state. Rajbhandari, P. Single cell analysis reveals immune cell-adipocyte crosstalk regulating the transcription of thermogenic adipocytes.

eLife , 8, e Ramirez, A. Single-cell transcriptional networks in differentiating preadipocytes suggest drivers associated with tissue heterogeneity. Burl, R. Deconstructing Adipogenesis Induced by β3-Adrenergic Receptor Activation with Single-Cell Expression Profiling. Henriques, F. Single-Cell RNA Profiling Reveals Adipocyte to Macrophage Signaling Sufficient to Enhance Thermogenesis.

Kumar, R. Single Cell Metabolomics: A Future Tool to Unmask Cellular Heterogeneity and Virus-Host Interaction in Context of Emerging Viral Diseases. Linke, V. A large-scale genome-lipid association map guides lipid identification.

Yore, M. Discovery of a class of endogenous mammalian lipids with anti-diabetic and anti-inflammatory effects. Cell , , — A lot of people are aware of thermogenesis, but many think that it applies solely to your metabolism. The Hypothalamus is situated in the centre of your brain and is responsible for a process known as thermoregulation finding a temperature balance.

When you are very cold your Hypothalamus or more accurately the primary motor centre that is found within the Hypothalamus can cause your muscles to shiver.

This can increase your metabolism five-fold and will raise your body temperature. This will lower your body temperature. Both of these are examples of thermoregulation. The purpose of thermoregulation is to keep your body temperature at the perfect balance, this is known as Homeostasis.

Thermoregulation is one control for Homeostasis but it is not the only one, the body also regulates blood glucose, calcium levels, the partial pressure of o2 and Co2, blood pressure etc The Thermic Effect of Food protein is best for weight loss.

The Snickers bar is calories 11g fat, 3g protein, 28g carbohydrates. The 11g of fat equals 99 calories fat is 9 calories per gram , the 3g of protein is 12 calories protein is 4 calories per gram , and the 28g of carbohydrates are calories carbs are also 4 calories per gram.

This comes to Remember, this is the low end of the scale. But even if you consider yourself sedentary, you are still underestimating how many calories you are burning. This is thanks to Of course exercising will burn a lot more calories than sitting at a desk typing an email, but the act of typing will still burn calories!

In other words you could probably manage 1. This form of activity is known as Non Exercise Activity Thermogenesis NEAT and it covers all forms of movement that are not exercise: walking, climbing stairs, doing the washing up, cooking, cleaning, even fidgeting whilst watching a movie.

The calories burned per activity are barely significant when looked at individually, but they add up to a lot of calories burned during the day. Some supplements are designed to have a thermic effect on the body, causing your resting RMR to increase.

This is literally additional calories being burned without the additional work, and can go a long way in burning that unwanted belly fat.

Yes, it is a real thing, but no it won't make you shed weight without effort. Thermogenic supplements are designed for people looking for an extra edge.

To push their bodies to the next level of esthetic achievement. To help them burn extra calories and get in even better shape. Thermogenic supplements are NOT designed for overweight individuals who have no intention of exercising or eating healthy.

The structure has the typical fold of a member of the SLC25 family. This uncouples oxidative phosphorylation , and the energy from the proton motive force is dissipated as heat rather than producing ATP from ADP, which would store chemical energy for the body's use.

Acetylcholine stimulates muscle to raise metabolic rate. The low demands of thermogenesis mean that free fatty acids draw, for the most part, on lipolysis as the method of energy production. A comprehensive list of human and mouse genes regulating cold-induced thermogenesis CIT in living animals in vivo or tissue samples ex vivo has been assembled [15] and is available in CITGeneDB.

The biological processes which allow for thermogenesis in animals did not evolve from a singular, common ancestor. However, while both clades are capable of performing thermogenesis, the biological processes involved are different. The reason that both avians and eutherians both developed the capacity to perform thermogenesis is a subject of ongoing study by evolutionary biologists , and two competing explanations have been proposed to explain why this character appears in both lineages.

This theory suggests that natural selection favored individuals with higher resting metabolic rates , and that as the metabolic capacity of birds and eutherians increased, they developed the capacity for endothermic thermogenesis.

Rather than animals developing the capacity to maintain high and stable body temperatures only to be able to thermoregulate without the aid of the environment, this theory suggests that thermogenesis is actually a by-product of natural selection for higher aerobic and metabolic capacities.

This theory proposes that the convergent evolution of thermogenesis in birds and eutherians is based on shared behavioral traits. Specifically, birds and eutherians both provide high levels of parental care to young offspring. This high level of care is theorized to give new born or hatched animals the opportunity to mature more rapidly because they have to expend less energy to satisfy their food, shelter, and temperature needs.

Despite both relying on similar explanations for the process by which organisms gained the capacity to perform non-shivering thermogenesis, neither of these explanations has secured a large enough consensus to be considered completely authoritative on convergent evolution of NST in birds and mammals, and scientists continue to conduct studies which support both positions.

Brown Adipose Tissue BAT thermogenesis is one of the two known forms of non-shivering thermogenesis NST. This type of heat-generation occurs only in eutherians, not in birds or other thermogenic organisms.

Because eutherians are the only clade which store brown adipose tissue, scientists previously thought that UCP1 evolved in conjunction with brown adipose tissue.

However, recent studies have shown that UCP1 can also be found in non-eutherians like fish, birds, and reptiles. Since this evolutionary split, though, UCP1 has evolved independently in eutherians, through a process which scientists believe was not driven by natural selection, but rather by neutral processes like genetic drift.

The second form of NST occurs in skeletal muscle. While eutherians use both BAT and skeletal muscle NST for thermogenesis, birds only use the latter form. This process has also been shown to occur in rare instances in fish.

Skeletal muscle NST might also be used to maintain body temperature in heterothermic mammals during states of torpor or hibernation.

The fact that skeletal muscle NST is common among eutherians during periods of torpor and hibernation further supports the theory that this form of thermogenesis is older than BAT NST.

This is because early eutherians would not have had the capacity for non-shivering thermogenesis as it currently exists, so they more frequently used torpor and hibernation as means of thermal regulation, relying on systems which, in theory, predate BAT NST.

However, there remains no consensus among evolutionary biologists on the order in which the two processes evolved, nor an exact timeframe for their evolution.

Non-shivering thermogenesis is regulated mainly by thyroid hormone and the sympathetic nervous system. Some hormones, such as norepinephrine and leptin , may stimulate thermogenesis by activating the sympathetic nervous system. Rising insulin levels after eating may be responsible for diet-induced thermogenesis thermic effect of food.

Barbara BodJan Nedergaard; Nonshivering thermogenesis and its adequate measurement in metabolic studies. J Exp Biol Tuermogenesis January ; Thernogenesis : — Alterations in nonshivering thermogenesis are presently discussed as being both potentially causative of and able to counteract obesity. However, the necessity for mammals to defend their body temperature means that the ambient temperature profoundly affects the outcome and interpretation of metabolic experiments. An adequate understanding and assessment of nonshivering thermogenesis is therefore paramount for metabolic studies.

Thermogenesis, the production of heat energy, is an essential component of the Thermogendsis repertoire to maintain body temperature during the challenge genrration low environmental temperature and plays a key generatiion in elevating body temperature during the febrile Garcinia cambogia for antioxidants to infection.

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Generatioj review summarizes the research leading to a model of the feedforward generaion pathway through which environmental cold Longevity and healthy aging strategies BAT EGCG and sun protection Thermogenesis and body heat generation includes the boyd on this gensration network anc the pyrogenic mediator, prostaglandin Thermogneesis 2to increase Thermogennesis temperature during hewt.

The Termogenesis thermal afferent circuit from cutaneous thermal receptors, through Roasted almond recipes thermosensory neurons in the dorsal horn of the spinal cord ascends to activate neurons in the lateral parabrachial nucleus which drive GABAergic interneurons in the preoptic area POA to inhibit warm-sensitive, inhibitory output neurons of the POA.

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Figure 1. Generatoin of the proposed neuroanatomical and neurotransmitter model bosy the Thermlgenesis thermoregulatory network and other CNS sites controlling brown adipose tissue BAT thermogenesis.

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Preoptic W-S neurons providing thermoregulatory control of BAT thermogenesis inhibit BAT sympathoexcitatory neurons in the dorsomedial hypothalamus DMH which, generatioh disinhibited during skin cooling, excite Age-defying moisturizers sympathetic premotor geneation in the rostral ventromedial medulla, including the rostral znd pallidus rRPathat project to BAT generarion preganglionic neurons SPN in the spinal intermediolateral nucleus Bodt.

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Orexinergic neurons in the perifornical lateral hypothalamus PeF-LH geeneration to the rRPa to Thermpgenesis the excitability of Cranberry holiday cocktails sympathetic premotor neurons.

Neurons in the paraventricular hypothalamic PVH nucleus exert an inhibitory influence on Ane thermogenesis, possibly genertion a GABAergic input Thermgoenesis BAT sympathetic premotor neurons in rRPa. Activation of neurons in the ventrolateral medulla VLM or in the nucleus of the solitary tract NTS produces an inhibition of BAT thermogenesis, potentially via a non-GABAergic input to rRPa or by activation of spinal inhibitory interneurons in the IML.

VGLUT3, vesicular glutamate transporter 3. As with other thermal effectors reviewed in Morrison, ; Morrison and Blessing,the thermoregulatory control of BAT thermogenesis occurs through a circuit that includes the pathways transmitting ambient temperature signals from thermal receptors in the skin to the hypothalamic networks that receive and integrate them with brain temperature information to activate efferent pathways to the thermal effectors.

Each of the synaptic integration sites in the core thermoregulatory pathway constitutes a potential site for the modulation of BAT thermogenesis by non-thermal signals. In contrast, the control of BAT thermogenesis by temperature-sensitive neurons in the brain constitutes a negative feedback reflex in that the warm-sensitive, preoptic area POA neurons activated by the increases in brain temperature resulting from stimulated BAT thermogenesis act, in turn, to inhibit sympathetic outflow to BAT.

The thermoregulatory system initiates defensive thermoregulatory responses in response to changes in skin temperature before they affect body core temperature.

In this way, exposure to a cold environment can leave core and brain temperatures unaffected or slightly increased Lomax et al. Such environmental temperature sensation is mediated through cutaneous thermoreceptors which are located in primary sensory nerve endings distributed in the skin.

The molecular mechanisms of cutaneous thermoreception appear to reside in the transient receptor potential TRP family of cation channels.

In addition, TRPM8 is activated by menthol McKemy et al. TRPV3 and TRPV4 are warm-sensitive TRP channels that are activated by innocuous warm temperatures and are expressed in keratinocytes in skin epidermis.

Compared to wild-type mice, mice lacking either TRPV3 or TRPV4 show altered behaviors in discriminating innocuous warm temperatures Lee et al. Peripheral or central administration of capsaicin induces hypothermia Jancso-Gabor et al.

Furthermore, administration of potent TRPV1 antagonists induces hyperthermia Gavva et al. Therefore, tonic activation of peripheral TRPV1, effected by non-thermal stimuli at body temperatures below the threshold for TRPV1 activation, could provide afferent signals to lower body temperature Romanovsky et al.

In addition to cutaneous thermoreception, thermoreceptive mechanisms exist in body core structures including the brain e.

The afferent fibers from cold and warm receptors in the abdominal viscera are included among the splanchnic and vagus nerve afferent fibers and their responses to temperature changes are similar to those of cutaneous thermoreceptors Riedel, ; Gupta et al.

Temperature changes in the spinal cord can affect the activity of thermoregulatory neurons in more rostral areas of the brain Guieu and Hardy, TRP channels that are located in the central endings of primary somatosensory fibers in the spinal dorsal horn Tominaga et al.

Thus, rather than responding directly to changes in environmental temperature, core body thermosensation could play a role a in setting the basal tone of thermoregulatory effector efferents including BAT thermogenesis, b in enhancing thermoregulatory responses in situations of extreme thermal environments when the feedforward thermoregulatory responses driven by changes in skin temperature have proven inadequate to prevent changes in brain or body core temperature, and c in responding to challenges to thermal homeostasis involving shifts in internal body temperature brought about by changes in metabolism e.

or by changes in internal temperature e. Primary thermal somatosensory fibers deliver thermal information to lamina I neurons in the spinal or trigeminal dorsal horn Craig, ; Figure 1.

Craig and colleagues have described thermoreceptor-specific cells responding linearly to graded, innocuous cooling or warming stimuli, and not being activated further in the noxious temperature range Andrew and Craig, ; Craig et al.

The spinothalamocortical pathway, in which second-order thermosensory neurons in lamina I ascend to synapse on thalamic neurons that, in turn, project to the primary somatosensory cortex, is responsible for conscious perception and discrimination of cutaneous temperature information Craig et al.

However, the spinothalamocortical pathway is not required to initiate or sustain involuntary thermoregulatory responses to environmental cold challenges, since thalamic lesions have no effect on sympathetic thermogenic responses to skin cooling Nakamura and Morrison, b.

However, spinothalamic and trigeminothalamic lamina I neurons do send collateral axons to the lateral parabrachial nucleus LPB Hylden et al.

Another group of afferents likely to influence BAT thermogenesis Niijima, arise from both BAT Bartness et al. What these afferents sense, the pathways through which this information is relayed centrally and how these adipose afferent signals might influence BAT thermogenesis remain interesting questions.

Neurons in the external lateral subnucleus LPBel of the LPB and projecting to the median subnucleus MnPO of the POA are activated following cold exposure Bratincsak and Palkovits, ; Nakamura and Morrison, bwhile those in the dorsal subnucleus LPBd are activated in response to skin warming Bratincsak and Palkovits, ; Nakamura and Morrison, The discharge rate of single, MnPO-projecting LPBel neurons recorded in vivo increased markedly in response to skin cooling in a manner paralleling the skin cooling-evoked increases in BAT SNA Nakamura and Morrison, b.

In contrast, single, MnPO-projecting LPBd neurons were excited by skin warming in parallel with the simultaneous inhibition of BAT SNA Nakamura and Morrison, The critical role of LPB neurons in transmitting cutaneous, and possibly visceral, thermal sensory information to the hypothalamus to drive BAT thermogenic responses is demonstrated by the elimination of BAT responses to alterations in skin temperature following experimental inactivation of local neurons or blockade of local glutamate receptors in the LPB Kobayashi and Osaka, ; Nakamura and Morrison, b.

Similarly, glutamate or other stimulations of LPBel or LPBd neurons can evoke BAT sympathetic and thermogenic responses that parallel those evoked during decreases or increases, respectively, in skin temperature Nakamura and Morrison, b Thus, both cool and warm cutaneous thermosensory signals that are transmitted from spinal dorsal horn or trigeminal neurons to the POA by separate populations of LPB neurons Figure 1 are essential for eliciting rapid responses in BAT thermogenesis to defend body temperature from a variety of thermal challenges.

Although nociceptive inputs play only a minor role Nakamura and Morrison, bwe do not know what other signals are integrated with cutaneous cold afferent inputs to LPBel neurons in the feedforward pathway contributing to drive BAT thermogenesis during environmental cold challenges. Within the neural circuits regulating body temperature, the hypothalamus, including the POA, occupies a pivotal position between the cutaneous sensation of ambient temperature and the motor pathways controlling the engagement of thermal effectors Figure 1.

Befitting its function as a central integrator of the many dimensions of homeostatic space, the hypothalamus is composed of several interconnected populations of neurons, receives a variety of signals relating to behavioral and emotional state, as well as the condition of the body and the interstitial fluid, and has outputs influencing emotional, behavioral, somatic, and autonomic responses.

Control of body temperature is but one of a myriad of interrelated homeostatic functions embedded in the hypothalamic matrix. Despite the anatomical and neurochemical complexity of this brain region, and the many factors that can influence body temperature regulation, considerable progress has been made in understanding the functional organization of the hypothalamic network that controls BAT thermogenesis.

Within the POA, feedforward, cutaneous cool signaling driving BAT thermogenesis is mediated by glutamatergic inputs from LPBel neurons to neurons in MnPO Figure 1. Stimulation of BAT thermogenesis by activation of LPBel neurons or by skin cooling is blocked by inhibiting neuronal activity in the MnPO Figure 2 or by antagonizing glutamate receptors in the MnPO Nakamura and Morrison, aband glutamatergic stimulation of MnPO neurons evokes increases in BAT SNA and BAT thermogenesis that are similar to cold-defensive BAT responses Nakamura and Morrison, a.

That the POA subregion receiving thermosensory cold signals is confined to the MnPO is supported by the findings that the projections from LPBel neurons activated by skin cooling terminate mainly in a median part of the POA Nakamura and Morrison, b and that glutamatergic stimulation or disinhibition of the MnPO with nanoinjections of NMDA or bicuculline, respectively, evokes physiological responses mimicking cold-defensive responses, while the same stimulation of the MPO or LPO does not Nakamura and Morrison, a.

Thus, activation of MnPO neurons is an essential step in the central mechanism for eliciting cold-defensive BAT thermogenesis to environmental cold challenges Figure 1. MnPO neurons receiving cutaneous thermal signals from LPB neurons also presumably receive other synaptic inputs that could influence the cutaneous thermal afferent regulation of BAT thermogenesis, although the sources of such inputs to these MnPO neurons are unknown.

The strong activation of BAT thermogenesis by local nanoinjections of bicuculline into MnPO Nakamura and Morrison, a suggests that one such input, at least in anesthetized rats, provides a tonic inhibition of skin cooling-responsive neurons in MnPO.

Figure 2. Inhibition of neurons in the median preoptic nucleus MnPO or blockade of GABA A receptors in the medial preoptic nucleus MPO prevents skin cooling-evoked BAT thermogenesis.

A Before and after injection of saline SAL vehicle into the MnPO [inset: typical injection site arrow in the MnPO; 3v, third ventricle; ox, optic chiasm; ac, anterior commissure], episodes of skin cooling evoke increases in BAT sympathetic nerve activity SNABAT temperature TBATexpired CO 2 Exp CO 2and heart rate HRwith no change in arterial pressure AP.

Following nanoinjection of the inhibitory transmitter, glycine GLYinto the MnPO, skin cooling no longer increases these thermoregulatory parameters.

Modified with permission from Nakamura and Morrison a. B The skin cooling-evoked increases in thermoregulatory parameters, including BAT SNA and TBAT, are unaffected by nanoinjection of saline vehicle into the MPO, but these increases are reversed by blockade of GABA A receptors in MPO with nanoinjection of bicuculline BIC.

Modified with permission from Nakamura and Morrison Stimulation of BAT thermogenesis in response to skin cooling is postulated to occur via a disinhibitory mechanism in which MnPO neurons receiving cutaneous cool signals from LPBel neurons provide a GABA input to the warm-sensitive, inhibitory projection neurons in the MPO Figure 1 to reduce their tonic activity, resulting in disinhibition of neurons in caudal brain regions whose excitation stimulates BAT thermogenesis for cold defense.

Consistent with this hypothesis, increases in BAT thermogenesis evoked by skin cooling Figure 2 or by stimulation of MnPO neurons are reversed completely by antagonizing GABA A receptors in the MPO Nakamura and Morrison, a.

The existence of GABAergic interneurons in the MnPO that innervate the MPO projection neurons is supported by the anatomical observations a that some MnPO neurons innervate the MPO Uschakov et al. The conceptual foundation of our current understanding of the role of the hypothalamus in normal body temperature regulation and in the elevated body temperature during fever is the existence of a class of hypothalamic neurons which have intrinsic temperature sensitivity: in the absence of synaptic inputs, their discharge frequency increases as the temperature of their local environment increases.

The neurophysiological mechanism underlying the thermosensitivity of warm-sensitive neurons in the POA is thought to reside in a warming-dependent facilitation of the rate of rise of a depolarizing prepotential, due to an heat-induced increase in the inactivation rate of an A-type potassium current, which shortens the intervals between action potentials and thereby increases their firing rates Boulant, a.

Warm-sensitivity could also arise from a heat-induced membrane depolarization that allows warm-sensitive neurons to reach their discharge threshold potential and then determines their discharge frequency Kobayashi et al. Although neurons whose spontaneous discharge frequency is altered by changing the temperature of their local environment exist throughout the CNS, those in the POA and anterior hypothalamus have been most intensely studied because thermoregulatory responses, perhaps with the exception of certain thermoregulatory behaviors Almeida et al.

The preeminent importance of central warm-sensitive neurons for the maintenance of normal body temperature can also be appreciated from the relative position of mammalian resting body temperatures well above the freezing point of water, but only a few degrees below the temperature at which proteins begin irreversible denaturation Romanovsky, Initial, in vivo recordings in the POA identified neurons with spontaneous discharge at thermoneutral temperatures that increased their discharge during local hypothalamic warming i.

The POA contains warm-sensitive neurons whose tonic discharge is also reduced by skin cooling and whose thermosensitivity to preoptic temperature is increased when the skin is cooled Boulant and Hardy, In subsequent recordings in the POA in hypothalamic slices, the majority of thermosensitive neurons were warm-sensitive Boulant and Dean, and the majority of these were GABAergic Lundius et al.

Further, either skin cooling or direct cooling of the local environment of POA neurons evokes sympathetic thermogenesis in BAT Imai-Matsumura et al. These findings are consistent with a model Figure 1 in which warm-sensitive POA neurons that are tonically active at thermoneutral temperatures, integrate cutaneous and local thermal information, and send inhibitory projections from the MPO to suppress BAT thermogenesis.

The observation that transection of the neuraxis immediately caudal to the POA increases BAT SNA and BAT thermogenesis Chen et al.
: Thermogenesis and body heat generation

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Lipopolysaccharide activates specific populations of hypothalamic and brainstem neurons that project to the spinal cord. Keywords: brown adipose tissue, thermogenesis, thermoregulation, sympathetic nerve activity, preoptic hypothalamus, fever, rostral raphe pallidus, rostral ventromedial medulla. Citation: Morrison SF, Madden CJ and Tupone D Central control of brown adipose tissue thermogenesis. doi: Received: 17 October ; Paper pending published: 12 November ; Accepted: 06 January ; Published online: 24 January Copyright: © Morrison, Madden and Tupone. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License , which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. Morrison, Neurological Surgery, Oregon Health and Science University, South West Sam Jackson Park Road, Portland, OR , USA. e-mail: morrisos ohsu. 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This article is part of the Research Topic Biology and therapeutic potential of brown adipose tissue View all 16 articles. Central Control of Brown Adipose Tissue Thermogenesis. Shaun F. Madden Domenico Tupone. Introduction Thermogenesis, the production of heat energy, is an essential component of the homeostatic repertoire to maintain body temperature during the challenge of low environmental temperature. Keywords: brown adipose tissue, thermogenesis, thermoregulation, sympathetic nerve activity, preoptic hypothalamus, fever, rostral raphe pallidus, rostral ventromedial medulla Citation: Morrison SF, Madden CJ and Tupone D Central control of brown adipose tissue thermogenesis. Edited by: Patrick Seale , University of Pennsylvania, USA. Reviewed by: Ralf Jockers , University of Paris, France Patrick Seale , University of Pennsylvania, USA. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item. Download as PDF Printable version. Process of heat production within organisms. Not to be confused with thermogeneration. This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: "Thermogenesis" — news · newspapers · books · scholar · JSTOR February Learn how and when to remove this template message. This section may be too technical for most readers to understand. Please help improve it to make it understandable to non-experts , without removing the technical details. December Learn how and when to remove this template message. Nature Communications. Bibcode : NatCo doi : PMC PMID Human Physiology Twelfth ed. McGraw Hill. PLOS Genetics. The FASEB Journal. Canadian Journal of Zoology. 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Thermogenesis - Wikipedia	The Snickers bar is calories 11g fat, 3g protein, 28g carbohydrates. The 11g of fat equals 99 calories fat is 9 calories per gram , the 3g of protein is 12 calories protein is 4 calories per gram , and the 28g of carbohydrates are calories carbs are also 4 calories per gram. This comes to Remember, this is the low end of the scale. But even if you consider yourself sedentary, you are still underestimating how many calories you are burning. This is thanks to Of course exercising will burn a lot more calories than sitting at a desk typing an email, but the act of typing will still burn calories! In other words you could probably manage 1. This form of activity is known as Non Exercise Activity Thermogenesis NEAT and it covers all forms of movement that are not exercise: walking, climbing stairs, doing the washing up, cooking, cleaning, even fidgeting whilst watching a movie. The calories burned per activity are barely significant when looked at individually, but they add up to a lot of calories burned during the day. Some supplements are designed to have a thermic effect on the body, causing your resting RMR to increase. This is literally additional calories being burned without the additional work, and can go a long way in burning that unwanted belly fat. Yes, it is a real thing, but no it won't make you shed weight without effort. Thermogenic supplements are designed for people looking for an extra edge. To push their bodies to the next level of esthetic achievement. To help them burn extra calories and get in even better shape. Thermogenic supplements are NOT designed for overweight individuals who have no intention of exercising or eating healthy. Our Transparent Labs PhysiqueSeries Fat Burner utilizes clinically tested ingredients at the dosages used in the clinical studies. Ingredients like caffeine, green tea extract, cayenne pepper, and salicin all have hundreds of studies showing efficacy in weight loss claims. Learn more about our Fat Burner and the studies for each ingredient used, by clicking here. Heat will evaporate from your body via sweat and respiration, your body will also transfer warm blood to superficial blood vessels i. ones close to the skin. This can lead to a flushed or reddened face. When it is too cold outside and you are trying to preserve heat, your body will also make changes. It will divert blood away from your extremities face, hands, feet etc and sends it to your core, which will then keep you better insulated. Your body can also increase your thermogenesis by shivering, this can greatly increase your metabolism and keep you warm as a result. It is for this reason that if you travel to a very cold climate you are required to increase your daily calorie intake due to the heightened metabolism you would automatically get. However this does not mean that you would lose a load of weight, as your NEAT levels would also lower to compensate. The problem is that whilst your calories would increase in a cold environment, your performance would suffer. The same issue would affect anyone trying to train in an overly hot environment, as Hettinga et al discovered in their study: training at high temperatures led to poorer performance in a 20 minute cycle [5]. The fact is that if you want to burn calories through exercise, then you should put your efforts into creating the optimal conditions in which to exercise — that will lead to you being able to work out harder, and therefore burn more calories. Trying to burn calories by wearing a sauna suit is like trying to run better by wearing concrete shoes, yes it is more difficult, but all it would do is prevent you from running properly! The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. Journal of the American College of Nutrition 23 5 : Thermic response to isoenergetic protein, carbohydrate or fat meals in lean and obese subjects. Clinical Science 65 : The Essentials of Sport and Exercise Nutrition 2nd ed. Precision Nutrition, Inc. pp Clearly, they have zones of comfort some degree higher than those of men Rohles, Thus, again, metabolic differences between men and women, examined under conditions with identical nominal temperatures, may in reality be secondary to differences in thermal responses rather than to more basic metabolic modalities. All mammals exposed to cold will initially shiver in order to elevate heat production Griggio, Thus, extensive periods of life in the cold would seem difficult and stressful. However, during the Second World War, cold-room food stores were invaded with mice that apparently lived there all their life, even had their young there and seemed to thrive well under conditions that would seem very unpleasant for all small mammals —10°C Barnett, That all of this would happen under conditions of constant shivering seemed unlikely. The effect of increased insulation on the thermoneutral zone. As seen, animals with a better insulation a smaller slope of the line must necessarily also obtain a broader thermoneutral zone, because the line must extrapolate to the same defended body temperature. What was unexpectedly observed in rodents in the s was that after a prolonged period in the cold, the animals ceased to shiver but retained an equally high metabolic rate Sellers et al. This would allow for a more comfortable life in the cold. As this elevated metabolism was observed to occur in the absence of measurable shivering, it was appropriately termed nonshivering thermogenesis. The mediator and site of this nonshivering thermogenesis were initially unknown. Starting from experiments originally directed at thyroid hormone effects Ring, , it turned out that the disappearance of shivering was accompanied by an increase in the thermogenic response to adrenergic stimulation, i. the mediator was norepinephrine noradrenaline , released from the sympathetic nervous system Hsieh and Carlson, ; Depocas, Consequently, it was concluded that it was possible to estimate the capacity for nonshivering thermogenesis in an animal by injecting norepinephrine into the animal when it was at its thermoneutral temperature. Although this technique indeed activates nonshivering thermogenesis by mimicking the release of norepinephrine from specific regions of the sympathetic nervous system, it also unavoidably activates other adrenergic receptors in the body. This leads to some elevation of metabolism and thus to an overestimate of the nonshivering thermogenic capacity, as will be discussed below. The organ generating nonshivering thermogenesis remained controversial long after the mediator was identified. Many researchers believed that the predominant site was skeletal muscle, mainly because of its large size and thus potential large capacity for heat production. Based on now classical studies by R. Smith in the s Smith, ; Smith and Hock, ; Cameron and Smith, ; Smith, ; Smith and Roberts, , a few scientists believed that brown adipose tissue was the main site of nonshivering thermogenesis. That brown adipose tissue could generate heat was not in question, but the magnitude and thus significance of the heat production were controversial, particularly considering the small size of the organ. The controversy was resolved by the blood flow studies of Foster and colleagues in the late s, which demonstrated massive blood flow increases to brown adipose tissue, both on cold exposure Foster and Frydman, and following norepinephrine injection Foster and Frydman, , with no increases in blood flow to skeletal muscle; the blood leaving brown adipose tissue was also observed to be practically depleted in oxygen. Since then, practically all rodent researchers have agreed that brown adipose tissue is — at least — the main site of nonshivering thermogenesis; some, such as we, would maintain that it is the only site. Concerning humans, the idea that nonshivering thermogenesis provided it exists originates from muscle has persisted, not least because it has been the general view that brown adipose tissue did not exist in adults. Very recent observations have altered this view reviewed in Nedergaard et al. We would consider it likely that, in humans too, all nonshivering thermogenesis emanates from brown adipose tissue. During the s and onwards, studies were also performed that showed that brown adipose tissue went through a process of cell proliferation and increased differentiation when an animal was kept in a cold environment Cameron and Smith, Hence, the growth of the tissue could be seen both as the reason and the rate-limiting step for the development of nonshivering thermogenesis. This growth of brown adipose tissue following prolonged cold exposure is termed recruitment. In addition to the increased cell proliferation Hunt and Hunt, ; Bukowiecki et al. The basic principles for heat production in brown adipose tissue. The brown-fat cells are stimulated by norepinephrine NE released from the sympathetic nervous system. The norepinephrine binds, as indicated, to its receptor in the plasma membrane, and through intracellular signalling processes, this leads to degradation of the triglycerides TG in the lipid droplets, and the released free fatty acids FFA interact with uncoupling protein-1 UCP1 and, through this, overcome the inhibition of UCP1 caused by cytosolic purine nucleotides such as ATP and ADP, GTP and GDP. This leads to respiration in the mitochondria that is uncoupled from ATP synthesis. All energy from the combustion of substrate food is therefore directly released as heat. Thus, classical nonshivering thermogenesis is a facultative meaning that it can be turned on and off within minutes , adaptive meaning that it needs weeks to develop form of thermogenesis that can be acutely induced by norepinephrine injection i. an adrenergic thermogenesis. In the s, the biochemical mechanism for heat production in brown adipose tissue was extensively investigated. It became apparent that the heat production occurred in the mitochondria as a consequence of a regulated uncoupling process mediated by a unique protein Nicholls, The protein was isolated in Lin and Klingenberg, and is now known as UCP1. In Fig. In resting cells, the activity of UCP1 is inhibited by bound purine nucleotides. When the cell is activated by norepinephrine, a lipolytic cascade is initiated that results in UCP1 activation. The exact mechanism of this activation is still not fully resolved Nedergaard et al. During early mammalian evolution, UCP1 developed rapidly Saito et al. UCP1 is principally found in all mammals — with the pig family being the only exception Berg et al. Pigs have secondarily lost the ability to express UCP1 and are thus incapable of nonshivering thermogenesis Mount, In our opinion, UCP1 is the only true thermogenic uncoupling protein, and the other proteins with similar names UCP2—5 have received their names based on homology in amino acid sequence, not on homology in function. To delineate the significance of brown adipose tissue under different physiological conditions, animals without brown adipose tissue would really be necessary. However, such animals have been difficult to generate, either by attempts to dissect away brown fat which cannot be done adequately as the tissue depots are found in so many places or by molecular means. However, because of the significance of UCP1 for the thermogenic mechanism of brown adipose tissue, a mouse with a genetic ablation of UCP1 Enerbäck et al. Therefore, with such a mouse as an experimental tool, many questions concerning the significance of brown adipose tissue heat production under different physiological conditions have now been stringently addressed. As anticipated, brown adipocytes isolated from UCP1-ablated mice do not respond to norepinephrine addition with an increase in oxygen consumption, i. they do not show adrenergic thermogenesis Matthias et al. However, the basal respiration of the cells is identical regardless of whether they possess UCP1. it does not allow for proton flux over the mitochondrial membrane when it is not directly stimulated. UCP1-ablated mice are viable and fertile. In agreement with the results from the isolated brown adipocytes, there are no differences in basal metabolic rate between mice with and without UCP1 Golozoubova et al. This confirms the tenet that UCP1 is not leaky and does not contribute to basal metabolic rate. The UCP1-ablated mice were initially observed to be unable to defend body temperature when transferred from normal animal house temperatures of approximately 23 to 5°C Enerbäck et al. Although at first sight, this appears to be the expected result if brown adipose tissue were to be ascribed a major role in nonshivering thermogenesis, it seems to be in contradiction to the tenet that mammals initially shiver to maintain body temperature. However, the outcome is understandable within this tenet. A mouse with an ablation in the UCP1 gene that has been living at normal animal house temperatures will have been unable to develop any capacity for thermogenesis in its brown adipose tissue because of the lack of UCP1. Its survival at 23°C has been dependent on the constant use of shivering to increase metabolism. If such an animal is transferred to 5°C, it will — unlike the wild-type animal — have no brown adipose tissue activity, and is therefore forced to rely entirely upon shivering to defend its body temperature. The capacity and endurance of the shivering prove to be inadequate, and gradually the body temperature of the UCP1-ablated animal therefore decreases. If a UCP1-ablated mouse is housed at an intermediate, cooler temperature, such as 18°C, it can then be transferred to 5°C and survive for prolonged periods Golozoubova et al. Similarly, if the ambient temperature is successively decreased 2°C day —1 , the UCP1-ablated mice survive in the cold Ukropec et al. It seemed initially possible that such cold-acclimated mice had developed an alternative means of nonshivering thermogenesis. However, measurements of electrical activity in muscle i. shivering showed that, in contrast to the case in wild-type mice, these UCP1-ablated mice shiver with the same intensity after several weeks in the cold as they do on the initiation of exposure to cold Golozoubova et al. They have thus not developed any alternative nonshivering thermogenesis. Simple visual inspection of the mice in the cold also makes it clear that whereas the cold-acclimated wild-type mice are comfortable in the cold and move around normally, principally similarly to behaviour at normal temperatures, the cold-acclimated UCP1-ablated mice remain in one position, in the nest if possible, curled up and visibly shivering. Thus, there is no evidence that an alternative mechanism for nonshivering thermogenesis has developed. Rather it would seem that the endurance capacity of the mouse for shivering has increased, and its muscles therefore do not become exhausted, which allows for the uninterrupted maintenance of shivering and, therefore, defence of body temperature. Alterations in muscle capacity are indeed observable in cold-acclimated UCP1-ablated mice, measurable as alterations in muscle mitochondria ATP-synthase capacity Shabalina et al. Thus, no other adaptive adrenergic mechanism of thermogenesis exists or is induced in these mice. We would therefore maintain that all classical nonshivering thermogenesis is located in brown adipose tissue. Until recently, it has been the general contention that there must be an alternative mechanism for heat production in muscle because it was believed that so-called thyroid hormone thermogenesis took place in muscle. However, it now seems likely that even thyroid hormone thermogenesis emanates from brown adipose tissue, due to thyroid hormone stimulation of the areas in the brain that control brown adipose tissue activity Sjögren et al. The metabolism of mice is often examined using a cold tolerance test. The mice may be able to cope with this challenge, or they may immediately or successively succumb to the cold Fig. This test indeed tests the cold tolerance of the mice, but does not examine nonshivering thermogenesis capacity, despite many implications of this in the literature. Typical results of a cold tolerance test. The animals may either be able to defend their body temperature indefinitely a or they may immediately b or after some time c succumb to the cold. In an acute situation such as this, the extra heat needed comes mainly from shivering, so this experiment mainly tests shivering endurance; however, factors such as animal insulation, heart and lung performance and delivery of substrate e. fatty acids from the white adipose tissue to the muscle may also be limiting for the cold tolerance. Therefore, this test does not explicitly examine the capacity for adaptive nonshivering thermogenesis, a process that takes weeks in the cold to develop. What it really tests is dependent on the previous thermal history of the animal, which determines the contribution of brown fat thermogenesis to total thermogenesis, and on the ability of an animal to elevate and maintain its total metabolism at the level needed to survive at the exposure temperature, through shivering. Regardless of whether an animal has brown adipose tissue, it must nonetheless elevate its total metabolism to the same extent in order to defend its body temperature. There are statements in the literature that imply that warming an animal through shivering thermogenesis should in some way be more energetically costly than heating it by nonshivering thermogenesis. This suggestion is difficult to reconcile with thermodynamics, and we are unaware of any experimental demonstration of this phenomenon. Indeed the metabolic rates of mice that produce their heat through shivering or nonshivering thermogenesis are identical Golozoubova et al. In a cold tolerance experiment, a fraction of the metabolic increase may be from brown fat and the remainder from shivering, or it may all derive from shivering. If the animal fails to maintain body temperature, it can be for any of a variety of reasons. The failure could indeed indicate an inadequacy in brown fat, but equally well an inadequacy in the ability to maintain shivering i. that there is a muscle problem , or that the heart or lungs are unable to meet the challenge of such a high elevation of metabolic rate. A further confounding issue with such a test, if it is used to investigate the significance of a particular gene in genetically modified mice, is that the gene of interest may alter the insulation of the mouse. As shown in Fig. If the gene of interest has actually made the fur more sparse, the mouse will, in practice, be exposed to a greater cold challenge and may cool more quickly than the wild-type mice. This could have been interpreted to mean that the gene of interest impairs brown fat thermogenesis but, as will be understood, this is clearly an inadequate interpretation. The outcome of a cold tolerance test is much influenced by the thermal prehistory of the mice. We can compare two such prehistories. If a wild-type mouse is first maintained at its thermoneutral temperature, approximately 30°C, and is then acutely transferred to 5°C, it will have to increase its metabolism immediately three- to fourfold see Fig. Some time later its body temperature and thus its metabolism may decrease Fig. Thus, the cold challenge is too great for the mouse to cope with: its ability to maintain a level of shivering that can counteract the cold for a prolonged period is insufficient. This can be interpreted in the way that at thermoneutral temperatures, the animal develops little or no brown adipose tissue. Consequently, on exposure to temperatures below thermoneutral, it will be entirely dependent on shivering thermogenesis for heat production. Constant shivering requires muscles with a capacity for constant endurance activity. Should this endurance ability fail, the animal has no other means to defend body temperature and its body temperature will decrease principally as illustrated in Fig. However Fig. normal animal house temperatures, for a prolonged period, it will recruit brown adipose tissue and UCP1 to the extent required to compensate for the temperature challenge represented by these temperatures. When such an animal is transferred to 5°C, it will keep full activity in its brown adipose tissue. However, this capacity will be insufficient, as it is adequate only for 23°C. Therefore, the animal will also shiver at a level necessary to compensate for the remainder of the cold demand Jansky et al. It thus has available the limited brown adipose tissue capacity plus its total shivering capacity. This means that it only needs to use a fraction of its shivering capacity and does not overtax this system. It can therefore cope with this sudden cold challenge. This illustrates one ecological advantage of developing brown fat thermogenic capacity: the ability to be prepared for successively decreasing temperatures. Effect of thermal prehistory on shivering demand. Animals pre-exposed to temperatures below thermoneutrality will develop a capacity for nonshivering thermogenesis NST adequate for that temperature. When the animals are acutely exposed to 4°C, the demand for shivering to compensate for the rest of the heat loss at 4°C is therefore reduced. Such animals will therefore manage better in a cold tolerance test Fig. Theoretical figure based on the data shown in Fig. Because it is norepinephrine that activates nonshivering thermogenesis, one means to evaluate the nonshivering thermogenic capacity of an animal is to treat it acutely with norepinephrine to mimic activation of the sympathetic nervous system Fig. Depending on the previous history of the animal, the magnitude of the response will vary. Under physiological circumstances, when an animal is exposed to cold, it will attempt to activate whatever brown fat it possesses. This is mediated by activation of the sympathetic nerves that directly innervate the brown adipose tissue depots Foster et al. This is thus not a generalized sympathetic activation but a highly localized one Cannon and Nedergaard, However, when norepinephrine is injected into an animal, a concentration must be given that is sufficiently high to mimic the local synaptic concentration Depocas et al. This results in all the cells of the animal being bathed in a high amount of norepinephrine. As essentially all cells possess adrenergic receptors that are coupled to metabolic responses of some type, an elevation of metabolism will ensue that is independent of brown fat and that does not occur under physiological circumstances. This response can therefore be seen as a purely pharmacological response and does not demonstrate any adaptive responsiveness. It leads to an overestimation of nonshivering thermogenic capacity because its magnitude can only be accurately evaluated in mice with a genetic ablation of UCP1. The magnitude of the adrenergic response in animals that have been housed at their thermoneutral temperature is a fairly close approximation Fig. Effect of cold acclimation on the thermogenic response to norepinephrine NE. NE was injected into wild-type mice which can produce heat in their brown adipose tissue and into UCP1-ablated mice UCP1 KO which are unable to do this ; the mice were acclimated to 30 or 4°C for at least 1 mo. There was no effect of the presence or absence of UCP1 with regard to the basal metabolic rate before norepinephrine injection. Acclimation to cold led to some increase in basal respiration probably related to the effects of the several-times larger food intake in these mice. Cold acclimation had no effect on the response to NE in the UCP1 KO mice. Only in the mice that possess UCP1 does acclimation to cold result in an increased response to NE. It corresponds to the development of adaptive nonshivering thermogenesis, and the increase due to cold acclimation represents the recruitment of brown adipose tissue i. the mice get more brown-fat cells, with more mitochondria and more UCP1 [V. Golozoubova, B. and J. Golozoubova et al. In animals with an extremely high capacity for nonshivering thermogenesis and with a good insulation, such a high heat production may be induced by norepinephrine that the animal becomes hyperthermic, as it cannot dissipate heat, and then this type of experiment cannot be undertaken. Nonshivering thermogenic capacity can be determined in awake, non-anaesthetized animals Jansky et al. Principally, an acute stress response is induced by the injection itself, in addition to the direct norepinephrine-induced thermogenesis. To improve the reproducibility of the measurements and decrease the number of animals required, anaesthetized animals can be studied. It is not possible to use inhalation anaesthetics as these inhibit brown fat activity Ohlson et al. The anaesthetized animal is placed in a small-volume measuring chamber at a temperature a few degrees higher than thermoneutral 33°C is needed for a mouse , in order to maintain its body temperature Golozoubova et al. After an adequate period of measurement to estimate the basal metabolic rate, the animal is removed and injected with norepinephrine and returned to the chamber. The metabolic rate will rise and plateau Fig. The increase over basal is the nonshivering thermogenic capacity plus the pharmacological response to norepinephrine. Basically, norepinephrine tests can therefore only be used to compare the difference in magnitude of the response between different conditions e. g warm- and cold-acclimated animals ; the absolute magnitude of nonshivering thermogenesis cannot be obtained by this method in itself. It is important to distinguish between adrenergic thermogenesis and nonshivering thermogenesis. is a thermoregulatory thermogenesis. In general, this is probably not the case. It is no surprise that different organs display increased oxygen consumption thermogenesis when stimulated with norepinephrine. In these organs, the cognate metabolic processes are stimulated, and any such stimulation leads to thermogenesis. Thus, norepinephrine stimulation of the salivary gland leads to increased oxygen consumption Terzic and Stoji, , as does stimulation of the liver Binet and Claret, These reactions have never been discussed to represent thermoregulatory thermogenesis; the heat is simply a by-product of the increased metabolism related to increased secretion, etc. Only because muscle is traditionally discussed as being a thermogenic organ are similar adrenergically induced responses in muscle discussed as representing a form of thermoregulatory thermogenesis. Importantly, these brown-fat-independent types of adrenergic thermogenesis have never been shown to be adaptive. This means that they are not recruited during acclimation to cold or adaptation to diet, and they are therefore not part of a thermoregulatory process. Particularly in humans, there are many results from studies using infusions of adrenergic agents and measurements of oxygen consumption Blaak et al. These studies are, for the reasons stated above, probably not relevant for the type of thermogenesis discussed here, i. thermoregulatory nonshivering thermogenesis or diet-induced thermogenesis. To our knowledge, there are no indications that this thermogenesis is adaptive. Additionally, there is the problem that the adrenergic concentrations achieved during infusion, particularly in humans, may be so low that only a hormonal action of adrenergic agonists is induced; i. the levels may not be high enough to reach the postsynaptic areas in a sufficiently high concentration. In that case, brown adipose tissue may not be stimulated at all. The problem with the pharmacological response to norepinephrine can to some extent be overcome by using a specific β 3 -adrenergic agonist, notably CL, As β 3 -adrenergic receptors are only found in high density in adipose tissues, and as white adipose tissue is nearly inert with respect to oxygen consumption, the response seen would mainly emanate from brown adipose tissue, i. However, the response may not represent the true capacity of brown adipose tissue because β 3 - and β 1 -adrenoreceptors may be needed to elicit the total β-adrenergic response, and there may be an α-adrenergic component Mohell et al. Thus, only with norepinephrine is it certain that the entire thermogenic response is induced. Metabolic chambers measure the rate of oxygen consumption, and the outcome is thus in litres of oxygen per unit time. This is an approximation of the total heat production but, because the thermal equivalent of an oxygen molecule is different when carbohydrate or fat is combusted, conversion factors depending on the respiratory quotient should be used to convert the oxygen consumption values to energy W. This is particularly important if the food composition is changed from carbohydrate to fat or during day-and-night measurements when the animals change from burning a mixed diet active phase to burning stored fat inactive phase. The problems occurring by expressing metabolism per kg body weight. The animals symbolized have similar amounts of normal tissue black but different amounts of white adipose tissue grey. Thus, to express metabolic rates per body weight or to any power of body weight leads to misleading conclusions. In studies of all types of metabolism, there is one major difficulty in interpretation and representation of the results: the denominator or the divisor, i. how the results should be expressed. If the animals are of the same size and body composition, there is no problem, but very often this is not the case. It may initially seem natural to express metabolism per gram body weight; however, in reality, animals are often studied that have become obese, e. due to a diet intervention or a genetic alteration. Such animals may have identical amounts of active lean tissue but are carrying expanded amounts of lipid around in their white adipose tissue Fig. Lipid as a chemical is totally metabolically inert, and in no way contributes to metabolism. However, if the metabolic rate is expressed per gram body weight, and one animal carries extra weight in the form of lipid, the metabolic rate expressed in this way will appear smaller in the obese animal. This is evidently not an adequate description. By contrast, if a treatment leads to leanness, the lipid carried around is less, the divisor is smaller and thus we have an explanation for leanness: enhanced thermogenesis Fig. Although these considerations would seem banal, the literature overflows with results calculated this way and conclusions based on these results. The problem has been repeatedly addressed, but still seems to persist Himms-Hagen, ; Butler and Kozak, In an apparently more advanced way, metabolic rates and thermogenic capacities can be expressed per gram body weight raised to some power. Most often the conversion is to grams raised to the power 0. Firstly, evidently this in no way eliminates the problem discussed above; lipid is still inert even if raised to any power. Secondly, the power 0. mice and elephants. It turns out that the metabolism increases in proportion to the body weight to the power 0. For mathematical reasons, the power raising makes nearly no difference if, for example, mice with only somewhat different body weights are compared, and it should therefore only be used for comparisons between species. Occasionally, the power 0. This is the geometrical relationship between the surface area and the volume weight of a sphere or cube. The power relationship is of significance if thermal balance is discussed — but to use it to express rates of metabolism implies that all metabolism is due to heat loss to the surroundings, which is of course not the case. The difference between the powers 0. What, then, is the solution to the dilemma of the divisor? The easiest — and in most circumstances most correct — solution is simply to give the results as per animal. A more sophisticated, and on occasion advantageous, solution is to express the rate per gram lean body mass. Even to express the metabolic rates per gram lean mass assumes that all lean mass in the body has an equal metabolic rate. This is not the case; therefore, although lean mass is a better approximation, it is not without its own problems. After all, if the modification studied should be causative of the development of obesity or protection against obesity , the altered metabolic rate should be present before the new phenotype becomes evident. Brown adipose tissue is an admirable defence mechanism against cold. It has an impressively high oxidative capacity and thermogenic activity per gram of tissue and provides chronically cold-exposed mammals with a comfortable means of defending body temperature. As pointed out above, in its absence, shivering will function but shivering is notably less comfortable than nonshivering thermogenesis and will impose restrictions on the animal's freedom of movement. Some 30 years ago, it was observed that a nonshivering thermogenic capacity could also be recruited by exposing rodents to so-called cafeteria diets or, later, to high-fat diets Rothwell and Stock, The mechanism of recruitment of brown adipose tissue under these conditions has not been clarified but it presumably involves activation of the sympathetic nervous system either directly by components in the diet as has been the general view or secondarily to the developing obesity as such. It was proposed that animals that could develop brown adipose tissue in this way could use its thermogenic capacity to combust excess energy in the diet and thus not become as obese as otherwise expected. Extensive studies by many groups have supported this view Cannon and Nedergaard, but see Maxwell et al. The magnitude of the increase in metabolic rate induced by injected norepinephrine is enhanced following dietary treatment, in a manner similar to that following cold acclimation i. classical nonshivering thermogenesis Rothwell and Stock, ; Feldmann et al. The increases seen are smaller, but it would seem to be an adaptive process, as is classical nonshivering thermogenesis. Also note that this metabolic increase is in addition to that caused by the direct metabolic costs of digesting the food. Whereas the purpose of classical nonshivering thermogenesis is clear, that of diet-induced thermogenesis is not equally evident. There are indications that the magnitude of diet-induced thermogenesis is related to the protein content of the diet. An adequate explanation for the development of diet-induced thermogenesis was proposed by Stock: if diets with inadequate protein or another essential nutrient content — i. unbalanced diets — were eaten to the extent that sufficient protein was ingested, a system had to exist to remove the excess of energy that this extra ingestion had incurred Stock, This system would thus be brown adipose tissue. Good experimental evidence for this hypothesis is still lacking. If an animal does use brown fat thermogenesis to regulate its amount of stored body fat, it would be reasonable to assume that in the absence of active brown fat such as in an animal lacking UCP1 , the animal would become obese, provided it maintained the same energy intake. It was therefore initially surprising perhaps even disappointing that the UCP1-ablated mice did not develop obesity Enerbäck et al. However, later studies performed in mice housed at their thermoneutral temperature showed a development of obesity even on a regular chow diet, and to a greater extent on a high-fat diet Feldmann et al. This indicates that even the very small amount of UCP1 present in the wild-type mice at thermoneutrality is actually effective in modulating body fat content, its absence is not compensated by other means, and the absence is sufficient for obesity to occur. Animals living at their thermoneutral temperatures are not under any cold stress and, therefore, clearly do not have UCP1 and brown fat for this reason. Brown fat is classically recruited in parallel with decreasing ambient temperatures. The presence of some active brown fat even at thermoneutrality can be taken to indicate that it indeed has a physiological function. Surprisingly, mice without UCP1 are protected against diet-obesity when studied under normal animal house conditions. The reason for this is still not clarified but this is not a unique outcome for UCP1-ablated mice. Even mice with UCP1 i. wild-type mice are protected against obesity if they are placed in a cold environment; however, the degree of cold needed for this protection is higher for wild-type than for UCP1-ablated mice Cannon and Nedergaard, Perhaps the most important reason to acquire a thermal understanding when approaching studies of metabolism is to not be misled by false positive observations and thus to invest scientific time and effort in metabolic phenomena that are secondary to thermal regulation rather than to truly altered metabolism. The risk of false positives. If, for example, a mutant mouse has fur with a decreased insulation, the slope of the thermal control curve becomes higher. If this mouse is only maintained and examined at normal temperature here 24°C , it will display a higher metabolism a than the control. The mutant thus appears to be hypermetabolic. In reality, it feels much colder than the wild-type mouse, i. it feels like the wild-type mouse would feel if it were shifted to a lower temperature where the same metabolism would be needed b ; that is it feels as if it were at 14°C c. It will therefore display all the features expected of mice at 14°C, e. All of these effects are, however, secondary to the animal feeling colder and will disappear if the mouse is kept and examined at thermoneutrality. Such examinations are rarely performed. As seen, the mouse of interest for thermoregulatory reasons necessarily shows an increased metabolism a thermogenesis , which wrongly suggests that it has an enhanced metabolism due to some metabolic pathway being modified. the appearance of UCP1-containing cells in white adipose tissue depots Xue et al. All of these observations would undoubtedly be formally correct, but when the thermoregulatory responses of the mouse are examined, these results become trivial in the sense that they are all consequences of decreased insulation. Thus, as indicated in Fig. In this example, all differences would thus be ascribable to the expected effects of feeling colder. The fact that this is more than a theoretical situation has been demonstrated several times recently. For example, a mouse without the fatty acid elongase Elovl3 demonstrated the above characteristics and was experimentally shown to have decreased insulation Westerberg et al. Similarly, the global absence of stearoyl CoA dehydrogenase 1 SCD1 leads to this type of apparently hypermetabolic phenotype Ntambi et al. Thus, the metabolic changes can be explained by the altered skin phenotype, the resultant increased heat loss and the effects of this resultant increased metabolism. The risk of false negatives. If a mutant animal truly has a decreased intrinsic metabolic rate but unchanged body temperature and insulation, it will not display a metabolic rate different from the wild type if kept and examined at normal temperatures a. Only if examined so as to establish the thermoneutral zone of the animal will the decreased metabolism become evident b. This is the case for thyroid receptor null mutants Golozoubova et al. It is likely that many mutants or treatments with true effects on intrinsic metabolism have been overlooked because they have only been examined under conditions where their metabolic rate is controlled by the ambient temperature. Other genetically modified mice have also been shown to exhibit changes in fur and skin properties together with resistance to diet-induced obesity; these include the global knock-out of acyl coenzyme A:diacylglycerol acyltransferase 1 DGAT1 Smith et al. Again, it is unlikely that these modifications truly affect intrinsic metabolism; rather, the outcome is due to thermoregulatory thermogenesis. In addition, mice that lack the thyroid hormone receptor α show an increased metabolism, etc.
Top bar navigation	Of course exercising will burn a lot more calories than sitting at a desk typing an email, but the act of typing will still burn calories! In other words you could probably manage 1. This form of activity is known as Non Exercise Activity Thermogenesis NEAT and it covers all forms of movement that are not exercise: walking, climbing stairs, doing the washing up, cooking, cleaning, even fidgeting whilst watching a movie. The calories burned per activity are barely significant when looked at individually, but they add up to a lot of calories burned during the day. Some supplements are designed to have a thermic effect on the body, causing your resting RMR to increase. This is literally additional calories being burned without the additional work, and can go a long way in burning that unwanted belly fat. Yes, it is a real thing, but no it won't make you shed weight without effort. Thermogenic supplements are designed for people looking for an extra edge. To push their bodies to the next level of esthetic achievement. To help them burn extra calories and get in even better shape. Thermogenic supplements are NOT designed for overweight individuals who have no intention of exercising or eating healthy. Our Transparent Labs PhysiqueSeries Fat Burner utilizes clinically tested ingredients at the dosages used in the clinical studies. Ingredients like caffeine, green tea extract, cayenne pepper, and salicin all have hundreds of studies showing efficacy in weight loss claims. Learn more about our Fat Burner and the studies for each ingredient used, by clicking here. Heat will evaporate from your body via sweat and respiration, your body will also transfer warm blood to superficial blood vessels i. ones close to the skin. This can lead to a flushed or reddened face. When it is too cold outside and you are trying to preserve heat, your body will also make changes. It will divert blood away from your extremities face, hands, feet etc and sends it to your core, which will then keep you better insulated. Your body can also increase your thermogenesis by shivering, this can greatly increase your metabolism and keep you warm as a result. It is for this reason that if you travel to a very cold climate you are required to increase your daily calorie intake due to the heightened metabolism you would automatically get. However this does not mean that you would lose a load of weight, as your NEAT levels would also lower to compensate. The problem is that whilst your calories would increase in a cold environment, your performance would suffer. The same issue would affect anyone trying to train in an overly hot environment, as Hettinga et al discovered in their study: training at high temperatures led to poorer performance in a 20 minute cycle [5]. The fact is that if you want to burn calories through exercise, then you should put your efforts into creating the optimal conditions in which to exercise — that will lead to you being able to work out harder, and therefore burn more calories. Trying to burn calories by wearing a sauna suit is like trying to run better by wearing concrete shoes, yes it is more difficult, but all it would do is prevent you from running properly! It results when the homeostatic control mechanisms of heat within the body malfunction, causing the body to lose heat faster than producing it. Normal body temperature is around 37°C It was then found that local differences were present, since heat production and heat loss vary considerably in different parts of the body, although the circulation of the blood tends to bring about a mean temperature of the internal parts. Hence it is important to identify the parts of the body that most closely reflect the temperature of the internal organs. Also, for such results to be comparable, the measurements must be conducted under comparable conditions. The rectum has traditionally been considered to reflect most accurately the temperature of internal parts, or in some cases of sex or species, the vagina , uterus or bladder. Some animals undergo one of various forms of dormancy where the thermoregulation process temporarily allows the body temperature to drop, thereby conserving energy. Examples include hibernating bears and torpor in bats. Thermoregulation in organisms runs along a spectrum from endothermy to ectothermy. Endotherms create most of their heat via metabolic processes and are colloquially referred to as warm-blooded. When the surrounding temperatures are cold, endotherms increase metabolic heat production to keep their body temperature constant, thus making the internal body temperature of an endotherm more or less independent of the temperature of the environment. They are colloquially referred to as cold-blooded despite the fact that body temperatures often stay within the same temperature ranges as warm-blooded animals. Ectotherms are the opposite of endotherms when it comes to regulating internal temperatures. In ectotherms, the internal physiological sources of heat are of negligible importance; the biggest factor that enables them to maintain adequate body temperatures is due to environmental influences. Living in areas that maintain a constant temperature throughout the year, like the tropics or the ocean, has enabled ectotherms to develop behavioral mechanisms that respond to external temperatures, such as sun-bathing to increase body temperature, or seeking the cover of shade to lower body temperature. To cope with low temperatures, some fish have developed the ability to remain functional even when the water temperature is below freezing; some use natural antifreeze or antifreeze proteins to resist ice crystal formation in their tissues. An example of behavioral adaptation is that of a lizard lying in the sun on a hot rock in order to heat through radiation and conduction. An endotherm is an animal that regulates its own body temperature, typically by keeping it at a constant level. To regulate body temperature, an organism may need to prevent heat gains in arid environments. Evaporation of water, either across respiratory surfaces or across the skin in those animals possessing sweat glands , helps in cooling body temperature to within the organism's tolerance range. Animals with a body covered by fur have limited ability to sweat, relying heavily on panting to increase evaporation of water across the moist surfaces of the lungs and the tongue and mouth. Mammals like cats, dogs and pigs, rely on panting or other means for thermal regulation and have sweat glands only in foot pads and snout. The sweat produced on pads of paws and on palms and soles mostly serves to increase friction and enhance grip. Birds also counteract overheating by gular fluttering , or rapid vibrations of the gular throat skin. Mammalian skin is much thicker than that of birds and often has a continuous layer of insulating fat beneath the dermis. In marine mammals, such as whales, or animals that live in very cold regions, such as the polar bears, this is called blubber. Dense coats found in desert endotherms also aid in preventing heat gain such as in the case of the camels. A cold weather strategy is to temporarily decrease metabolic rate, decreasing the temperature difference between the animal and the air and thereby minimizing heat loss. Furthermore, having a lower metabolic rate is less energetically expensive. Many animals survive cold frosty nights through torpor , a short-term temporary drop in body temperature. Organisms, when presented with the problem of regulating body temperature, have not only behavioural, physiological, and structural adaptations but also a feedback system to trigger these adaptations to regulate temperature accordingly. The main features of this system are stimulus, receptor, modulator, effector and then the feedback of the newly adjusted temperature to the stimulus. This cyclical process aids in homeostasis. Homeothermy and poikilothermy refer to how stable an organism's deep-body temperature is. Most endothermic organisms are homeothermic, like mammals. However, animals with facultative endothermy are often poikilothermic, meaning their temperature can vary considerably. Most fish are ectotherms, as most of their heat comes from the surrounding water. However, almost all fish are poikilothermic. By numerous observations upon humans and other animals, John Hunter showed that the essential difference between the so-called warm-blooded and cold-blooded animals lies in observed constancy of the temperature of the former, and the observed variability of the temperature of the latter. Almost all birds and mammals have a high temperature almost constant and independent of that of the surrounding air homeothermy. Almost all other animals display a variation of body temperature, dependent on their surroundings poikilothermy. Thermoregulation in both ectotherms and endotherms is controlled mainly by the preoptic area of the anterior hypothalamus. In cold environments, birds and mammals employ the following adaptations and strategies to minimize heat loss:. In warm environments, birds and mammals employ the following adaptations and strategies to maximize heat loss:. As in other mammals, thermoregulation is an important aspect of human homeostasis. Most body heat is generated in the deep organs, especially the liver, brain, and heart, and in contraction of skeletal muscles. High temperatures pose serious stresses for the human body, placing it in great danger of injury or even death. For example, one of the most common reactions to hot temperatures is heat exhaustion, which is an illness that could happen if one is exposed to high temperatures, resulting in some symptoms such as dizziness, fainting, or a rapid heartbeat. Scattered throughout the body in both peripheral and central nervous systems, these nerve cells are sensitive to changes in temperature and are able to provide useful information to the hypothalamus through the process of negative feedback, thus maintaining a constant core temperature. There are four avenues of heat loss: evaporation, convection, conduction, and radiation. If skin temperature is greater than that of the surrounding air temperature, the body can lose heat by convection and conduction. However, if air temperature of the surroundings is greater than that of the skin, the body gains heat by convection and conduction. In such conditions, the only means by which the body can rid itself of heat is by evaporation. So, when the surrounding temperature is higher than the skin temperature, anything that prevents adequate evaporation will cause the internal body temperature to rise. sports , evaporation becomes the main avenue of heat loss. Thermoregulation is also an integral part of a reptile's life, specifically lizards such as Microlophus occipitalis and Ctenophorus decresii who must change microhabitats to keep a constant body temperature. Thermogenesis occurs in the flowers of many plants in the family Araceae as well as in cycad cones. Heat is produced by breaking down the starch that was stored in their roots, [30] which requires the consumption of oxygen at a rate approaching that of a flying hummingbird. One possible explanation for plant thermoregulation is to provide protection against cold temperature. For example, the skunk cabbage is not frost-resistant, yet it begins to grow and flower when there is still snow on the ground. Some plants are known to protect themselves against colder temperatures using antifreeze proteins. This occurs in wheat Triticum aestivum , potatoes Solanum tuberosum and several other angiosperm species. Animals other than humans regulate and maintain their body temperature with physiological adjustments and behavior. Desert lizards are ectotherms, and therefore are unable to regulate their internal temperature themselves. To regulate their internal temperature, many lizards relocate themselves to a more environmentally favorable location. They may do this in the morning only by raising their head from its burrow and then exposing their entire body. By basking in the sun, the lizard absorbs solar heat. It may also absorb heat by conduction from heated rocks that have stored radiant solar energy. To lower their temperature, lizards exhibit varied behaviors. Sand seas, or ergs , produce up to They also go to their burrows to avoid cooling when the temperature falls. Aquatic animals can also regulate their temperature behaviorally by changing their position in the thermal gradient. Animals also engage in kleptothermy in which they share or steal each other's body warmth. Kleptothermy is observed, particularly amongst juveniles, in endotherms such as bats [35] and birds such as the mousebird [36] and emperor penguin [37]. This allows the individuals to increase their thermal inertia as with gigantothermy and so reduce heat loss. Other animals exploit termite mounds. Some animals living in cold environments maintain their body temperature by preventing heat loss. Their fur grows more densely to increase the amount of insulation. Some animals are regionally heterothermic and are able to allow their less insulated extremities to cool to temperatures much lower than their core temperature—nearly to 0 °C 32 °F. This minimizes heat loss through less insulated body parts, like the legs, feet or hooves , and nose. Different species of Drosophila found in the Sonoran Desert will exploit different species of cacti based on the thermotolerance differences between species and hosts. For example, Drosophila mettleri is found in cacti like the saguaro and senita ; these two cacti remain cool by storing water. Over time, the genes selecting for higher heat tolerance were reduced in the population due to the cooler host climate the fly is able to exploit. Some flies, such as Lucilia sericata , lay their eggs en masse. The resulting group of larvae, depending on its size, is able to thermoregulate and keep itself at the optimum temperature for development. Koalas also can behaviorally thermoregulate by seeking out cooler portions of trees on hot days. They preferentially wrap themselves around the coolest portions of trees, typically near the bottom, to increase their passive radiation of internal body heat. To cope with limited food resources and low temperatures, some mammals hibernate during cold periods. To remain in "stasis" for long periods, these animals build up brown fat reserves and slow all body functions. True hibernators e. Some bats are true hibernators and rely upon a rapid, non-shivering thermogenesis of their brown fat deposit to bring them out of hibernation. Estivation is similar to hibernation, however, it usually occurs in hot periods to allow animals to avoid high temperatures and desiccation. Both terrestrial and aquatic invertebrate and vertebrates enter into estivation. Examples include lady beetles Coccinellidae , [43] North American desert tortoises , crocodiles , salamanders , cane toads , [44] and the water-holding frog. Daily torpor occurs in small endotherms like bats and hummingbirds , which temporarily reduces their high metabolic rates to conserve energy. Previously, average oral temperature for healthy adults had been considered In Poland and Russia, the temperature had been measured axillarily under the arm. Recent studies suggest that the average temperature for healthy adults is Variations one standard deviation from three other studies are:. Measured temperature varies according to thermometer placement, with rectal temperature being 0. In humans, a diurnal variation has been observed dependent on the periods of rest and activity, lowest at 11 p. and peaking at 10 a. Monkeys also have a well-marked and regular diurnal variation of body temperature that follows periods of rest and activity, and is not dependent on the incidence of day and night; nocturnal monkeys reach their highest body temperature at night and lowest during the day. Sutherland Simpson and J. This model of thermogenesis refers to the heat generation reaction by brown adipose tissue. The body's processes of cellular respiration and oxidative phosphorylation result in the energy originally intended for ATP synthesis being used to produce heat. Non-shivering thermogenesis occurs when the body is exposed to cool air at a temperature of approx. In a nutshell, it refers to the increased production of heat due to the consumption of a meal. The organism must use the appropriate amount of energy to efficiently digest the provided macronutrients, but not only that. Energy is also used for a number of other functions related to nutrition, such as absorption and assimilation of active ingredients and their appropriate storage. At this point it is worth mentioning that nutrients have a TEF thermic effect of food coefficient, which influences the occurrence of postprandial thermogenesis. The consumption of certain foods and the active substances they contain has a valuable effect on increasing thermogenesis. These include products with a spicy aftertaste:. These substances are included in fat tissue burners produced by Olimp Sport Nutrition. The products contain highly standardised extracts and optimally selected proportions of individual ingredients, which ensure optimal and effective action to increase thermogenesis. The products have been produced in the form of handy capsules and tablets, and all ingredients have been obtained from high class raw materials which have been subjected to microbiological purity analysis. Language United kingdom. Home nutrition What is thermogenesis and what is its importance for the body? The information below is required for social login. Please complete your information below to creat an account. First Name. Last Name.
Video Upload Options	Process of heat production within organisms. Not to be confused with thermogeneration. This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Find sources: "Thermogenesis" — news · newspapers · books · scholar · JSTOR February Learn how and when to remove this template message. This section may be too technical for most readers to understand. Please help improve it to make it understandable to non-experts , without removing the technical details. December Learn how and when to remove this template message. Nature Communications. Bibcode : NatCo doi : PMC PMID Human Physiology Twelfth ed. McGraw Hill. PLOS Genetics. The FASEB Journal. Canadian Journal of Zoology. Physiological Reviews. S2CID Trends in Biochemical Sciences. June Science Advances. Bibcode : SciA The Journal of Experimental Biology. November FEBS Letters. 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However, during the Second World War, cold-room food stores were invaded with mice that apparently lived there all their life, even had their young there and seemed to thrive well under conditions that would seem very unpleasant for all small mammals —10°C Barnett, That all of this would happen under conditions of constant shivering seemed unlikely. The effect of increased insulation on the thermoneutral zone. As seen, animals with a better insulation a smaller slope of the line must necessarily also obtain a broader thermoneutral zone, because the line must extrapolate to the same defended body temperature. What was unexpectedly observed in rodents in the s was that after a prolonged period in the cold, the animals ceased to shiver but retained an equally high metabolic rate Sellers et al. This would allow for a more comfortable life in the cold. As this elevated metabolism was observed to occur in the absence of measurable shivering, it was appropriately termed nonshivering thermogenesis. The mediator and site of this nonshivering thermogenesis were initially unknown. Starting from experiments originally directed at thyroid hormone effects Ring, , it turned out that the disappearance of shivering was accompanied by an increase in the thermogenic response to adrenergic stimulation, i. the mediator was norepinephrine noradrenaline , released from the sympathetic nervous system Hsieh and Carlson, ; Depocas, Consequently, it was concluded that it was possible to estimate the capacity for nonshivering thermogenesis in an animal by injecting norepinephrine into the animal when it was at its thermoneutral temperature. Although this technique indeed activates nonshivering thermogenesis by mimicking the release of norepinephrine from specific regions of the sympathetic nervous system, it also unavoidably activates other adrenergic receptors in the body. This leads to some elevation of metabolism and thus to an overestimate of the nonshivering thermogenic capacity, as will be discussed below. The organ generating nonshivering thermogenesis remained controversial long after the mediator was identified. Many researchers believed that the predominant site was skeletal muscle, mainly because of its large size and thus potential large capacity for heat production. Based on now classical studies by R. Smith in the s Smith, ; Smith and Hock, ; Cameron and Smith, ; Smith, ; Smith and Roberts, , a few scientists believed that brown adipose tissue was the main site of nonshivering thermogenesis. That brown adipose tissue could generate heat was not in question, but the magnitude and thus significance of the heat production were controversial, particularly considering the small size of the organ. The controversy was resolved by the blood flow studies of Foster and colleagues in the late s, which demonstrated massive blood flow increases to brown adipose tissue, both on cold exposure Foster and Frydman, and following norepinephrine injection Foster and Frydman, , with no increases in blood flow to skeletal muscle; the blood leaving brown adipose tissue was also observed to be practically depleted in oxygen. Since then, practically all rodent researchers have agreed that brown adipose tissue is — at least — the main site of nonshivering thermogenesis; some, such as we, would maintain that it is the only site. Concerning humans, the idea that nonshivering thermogenesis provided it exists originates from muscle has persisted, not least because it has been the general view that brown adipose tissue did not exist in adults. Very recent observations have altered this view reviewed in Nedergaard et al. We would consider it likely that, in humans too, all nonshivering thermogenesis emanates from brown adipose tissue. During the s and onwards, studies were also performed that showed that brown adipose tissue went through a process of cell proliferation and increased differentiation when an animal was kept in a cold environment Cameron and Smith, Hence, the growth of the tissue could be seen both as the reason and the rate-limiting step for the development of nonshivering thermogenesis. This growth of brown adipose tissue following prolonged cold exposure is termed recruitment. In addition to the increased cell proliferation Hunt and Hunt, ; Bukowiecki et al. The basic principles for heat production in brown adipose tissue. The brown-fat cells are stimulated by norepinephrine NE released from the sympathetic nervous system. The norepinephrine binds, as indicated, to its receptor in the plasma membrane, and through intracellular signalling processes, this leads to degradation of the triglycerides TG in the lipid droplets, and the released free fatty acids FFA interact with uncoupling protein-1 UCP1 and, through this, overcome the inhibition of UCP1 caused by cytosolic purine nucleotides such as ATP and ADP, GTP and GDP. This leads to respiration in the mitochondria that is uncoupled from ATP synthesis. All energy from the combustion of substrate food is therefore directly released as heat. Thus, classical nonshivering thermogenesis is a facultative meaning that it can be turned on and off within minutes , adaptive meaning that it needs weeks to develop form of thermogenesis that can be acutely induced by norepinephrine injection i. an adrenergic thermogenesis. In the s, the biochemical mechanism for heat production in brown adipose tissue was extensively investigated. It became apparent that the heat production occurred in the mitochondria as a consequence of a regulated uncoupling process mediated by a unique protein Nicholls, The protein was isolated in Lin and Klingenberg, and is now known as UCP1. In Fig. In resting cells, the activity of UCP1 is inhibited by bound purine nucleotides. When the cell is activated by norepinephrine, a lipolytic cascade is initiated that results in UCP1 activation. The exact mechanism of this activation is still not fully resolved Nedergaard et al. During early mammalian evolution, UCP1 developed rapidly Saito et al. UCP1 is principally found in all mammals — with the pig family being the only exception Berg et al. Pigs have secondarily lost the ability to express UCP1 and are thus incapable of nonshivering thermogenesis Mount, In our opinion, UCP1 is the only true thermogenic uncoupling protein, and the other proteins with similar names UCP2—5 have received their names based on homology in amino acid sequence, not on homology in function. To delineate the significance of brown adipose tissue under different physiological conditions, animals without brown adipose tissue would really be necessary. However, such animals have been difficult to generate, either by attempts to dissect away brown fat which cannot be done adequately as the tissue depots are found in so many places or by molecular means. However, because of the significance of UCP1 for the thermogenic mechanism of brown adipose tissue, a mouse with a genetic ablation of UCP1 Enerbäck et al. Therefore, with such a mouse as an experimental tool, many questions concerning the significance of brown adipose tissue heat production under different physiological conditions have now been stringently addressed. As anticipated, brown adipocytes isolated from UCP1-ablated mice do not respond to norepinephrine addition with an increase in oxygen consumption, i. they do not show adrenergic thermogenesis Matthias et al. However, the basal respiration of the cells is identical regardless of whether they possess UCP1. it does not allow for proton flux over the mitochondrial membrane when it is not directly stimulated. UCP1-ablated mice are viable and fertile. In agreement with the results from the isolated brown adipocytes, there are no differences in basal metabolic rate between mice with and without UCP1 Golozoubova et al. This confirms the tenet that UCP1 is not leaky and does not contribute to basal metabolic rate. The UCP1-ablated mice were initially observed to be unable to defend body temperature when transferred from normal animal house temperatures of approximately 23 to 5°C Enerbäck et al. Although at first sight, this appears to be the expected result if brown adipose tissue were to be ascribed a major role in nonshivering thermogenesis, it seems to be in contradiction to the tenet that mammals initially shiver to maintain body temperature. However, the outcome is understandable within this tenet. A mouse with an ablation in the UCP1 gene that has been living at normal animal house temperatures will have been unable to develop any capacity for thermogenesis in its brown adipose tissue because of the lack of UCP1. Its survival at 23°C has been dependent on the constant use of shivering to increase metabolism. If such an animal is transferred to 5°C, it will — unlike the wild-type animal — have no brown adipose tissue activity, and is therefore forced to rely entirely upon shivering to defend its body temperature. The capacity and endurance of the shivering prove to be inadequate, and gradually the body temperature of the UCP1-ablated animal therefore decreases. If a UCP1-ablated mouse is housed at an intermediate, cooler temperature, such as 18°C, it can then be transferred to 5°C and survive for prolonged periods Golozoubova et al. Similarly, if the ambient temperature is successively decreased 2°C day —1 , the UCP1-ablated mice survive in the cold Ukropec et al. It seemed initially possible that such cold-acclimated mice had developed an alternative means of nonshivering thermogenesis. However, measurements of electrical activity in muscle i. shivering showed that, in contrast to the case in wild-type mice, these UCP1-ablated mice shiver with the same intensity after several weeks in the cold as they do on the initiation of exposure to cold Golozoubova et al. They have thus not developed any alternative nonshivering thermogenesis. Simple visual inspection of the mice in the cold also makes it clear that whereas the cold-acclimated wild-type mice are comfortable in the cold and move around normally, principally similarly to behaviour at normal temperatures, the cold-acclimated UCP1-ablated mice remain in one position, in the nest if possible, curled up and visibly shivering. Thus, there is no evidence that an alternative mechanism for nonshivering thermogenesis has developed. Rather it would seem that the endurance capacity of the mouse for shivering has increased, and its muscles therefore do not become exhausted, which allows for the uninterrupted maintenance of shivering and, therefore, defence of body temperature. Alterations in muscle capacity are indeed observable in cold-acclimated UCP1-ablated mice, measurable as alterations in muscle mitochondria ATP-synthase capacity Shabalina et al. Thus, no other adaptive adrenergic mechanism of thermogenesis exists or is induced in these mice. We would therefore maintain that all classical nonshivering thermogenesis is located in brown adipose tissue. Until recently, it has been the general contention that there must be an alternative mechanism for heat production in muscle because it was believed that so-called thyroid hormone thermogenesis took place in muscle. However, it now seems likely that even thyroid hormone thermogenesis emanates from brown adipose tissue, due to thyroid hormone stimulation of the areas in the brain that control brown adipose tissue activity Sjögren et al. The metabolism of mice is often examined using a cold tolerance test. The mice may be able to cope with this challenge, or they may immediately or successively succumb to the cold Fig. This test indeed tests the cold tolerance of the mice, but does not examine nonshivering thermogenesis capacity, despite many implications of this in the literature. Typical results of a cold tolerance test. The animals may either be able to defend their body temperature indefinitely a or they may immediately b or after some time c succumb to the cold. In an acute situation such as this, the extra heat needed comes mainly from shivering, so this experiment mainly tests shivering endurance; however, factors such as animal insulation, heart and lung performance and delivery of substrate e. fatty acids from the white adipose tissue to the muscle may also be limiting for the cold tolerance. Therefore, this test does not explicitly examine the capacity for adaptive nonshivering thermogenesis, a process that takes weeks in the cold to develop. What it really tests is dependent on the previous thermal history of the animal, which determines the contribution of brown fat thermogenesis to total thermogenesis, and on the ability of an animal to elevate and maintain its total metabolism at the level needed to survive at the exposure temperature, through shivering. Regardless of whether an animal has brown adipose tissue, it must nonetheless elevate its total metabolism to the same extent in order to defend its body temperature. There are statements in the literature that imply that warming an animal through shivering thermogenesis should in some way be more energetically costly than heating it by nonshivering thermogenesis. This suggestion is difficult to reconcile with thermodynamics, and we are unaware of any experimental demonstration of this phenomenon. Indeed the metabolic rates of mice that produce their heat through shivering or nonshivering thermogenesis are identical Golozoubova et al. In a cold tolerance experiment, a fraction of the metabolic increase may be from brown fat and the remainder from shivering, or it may all derive from shivering. If the animal fails to maintain body temperature, it can be for any of a variety of reasons. The failure could indeed indicate an inadequacy in brown fat, but equally well an inadequacy in the ability to maintain shivering i. that there is a muscle problem , or that the heart or lungs are unable to meet the challenge of such a high elevation of metabolic rate. A further confounding issue with such a test, if it is used to investigate the significance of a particular gene in genetically modified mice, is that the gene of interest may alter the insulation of the mouse. As shown in Fig. If the gene of interest has actually made the fur more sparse, the mouse will, in practice, be exposed to a greater cold challenge and may cool more quickly than the wild-type mice. This could have been interpreted to mean that the gene of interest impairs brown fat thermogenesis but, as will be understood, this is clearly an inadequate interpretation. The outcome of a cold tolerance test is much influenced by the thermal prehistory of the mice. We can compare two such prehistories. If a wild-type mouse is first maintained at its thermoneutral temperature, approximately 30°C, and is then acutely transferred to 5°C, it will have to increase its metabolism immediately three- to fourfold see Fig. Some time later its body temperature and thus its metabolism may decrease Fig. Thus, the cold challenge is too great for the mouse to cope with: its ability to maintain a level of shivering that can counteract the cold for a prolonged period is insufficient. This can be interpreted in the way that at thermoneutral temperatures, the animal develops little or no brown adipose tissue. Consequently, on exposure to temperatures below thermoneutral, it will be entirely dependent on shivering thermogenesis for heat production. Constant shivering requires muscles with a capacity for constant endurance activity. Should this endurance ability fail, the animal has no other means to defend body temperature and its body temperature will decrease principally as illustrated in Fig. However Fig. normal animal house temperatures, for a prolonged period, it will recruit brown adipose tissue and UCP1 to the extent required to compensate for the temperature challenge represented by these temperatures. When such an animal is transferred to 5°C, it will keep full activity in its brown adipose tissue. However, this capacity will be insufficient, as it is adequate only for 23°C. Therefore, the animal will also shiver at a level necessary to compensate for the remainder of the cold demand Jansky et al. It thus has available the limited brown adipose tissue capacity plus its total shivering capacity. This means that it only needs to use a fraction of its shivering capacity and does not overtax this system. It can therefore cope with this sudden cold challenge. This illustrates one ecological advantage of developing brown fat thermogenic capacity: the ability to be prepared for successively decreasing temperatures. Effect of thermal prehistory on shivering demand. Animals pre-exposed to temperatures below thermoneutrality will develop a capacity for nonshivering thermogenesis NST adequate for that temperature. When the animals are acutely exposed to 4°C, the demand for shivering to compensate for the rest of the heat loss at 4°C is therefore reduced. Such animals will therefore manage better in a cold tolerance test Fig. Theoretical figure based on the data shown in Fig. Because it is norepinephrine that activates nonshivering thermogenesis, one means to evaluate the nonshivering thermogenic capacity of an animal is to treat it acutely with norepinephrine to mimic activation of the sympathetic nervous system Fig. Depending on the previous history of the animal, the magnitude of the response will vary. Under physiological circumstances, when an animal is exposed to cold, it will attempt to activate whatever brown fat it possesses. This is mediated by activation of the sympathetic nerves that directly innervate the brown adipose tissue depots Foster et al. This is thus not a generalized sympathetic activation but a highly localized one Cannon and Nedergaard, However, when norepinephrine is injected into an animal, a concentration must be given that is sufficiently high to mimic the local synaptic concentration Depocas et al. This results in all the cells of the animal being bathed in a high amount of norepinephrine. As essentially all cells possess adrenergic receptors that are coupled to metabolic responses of some type, an elevation of metabolism will ensue that is independent of brown fat and that does not occur under physiological circumstances. This response can therefore be seen as a purely pharmacological response and does not demonstrate any adaptive responsiveness. It leads to an overestimation of nonshivering thermogenic capacity because its magnitude can only be accurately evaluated in mice with a genetic ablation of UCP1. The magnitude of the adrenergic response in animals that have been housed at their thermoneutral temperature is a fairly close approximation Fig. Effect of cold acclimation on the thermogenic response to norepinephrine NE. NE was injected into wild-type mice which can produce heat in their brown adipose tissue and into UCP1-ablated mice UCP1 KO which are unable to do this ; the mice were acclimated to 30 or 4°C for at least 1 mo. There was no effect of the presence or absence of UCP1 with regard to the basal metabolic rate before norepinephrine injection. Acclimation to cold led to some increase in basal respiration probably related to the effects of the several-times larger food intake in these mice. Cold acclimation had no effect on the response to NE in the UCP1 KO mice. Only in the mice that possess UCP1 does acclimation to cold result in an increased response to NE. It corresponds to the development of adaptive nonshivering thermogenesis, and the increase due to cold acclimation represents the recruitment of brown adipose tissue i. the mice get more brown-fat cells, with more mitochondria and more UCP1 [V. Golozoubova, B. and J. Golozoubova et al. In animals with an extremely high capacity for nonshivering thermogenesis and with a good insulation, such a high heat production may be induced by norepinephrine that the animal becomes hyperthermic, as it cannot dissipate heat, and then this type of experiment cannot be undertaken. Nonshivering thermogenic capacity can be determined in awake, non-anaesthetized animals Jansky et al. Principally, an acute stress response is induced by the injection itself, in addition to the direct norepinephrine-induced thermogenesis. To improve the reproducibility of the measurements and decrease the number of animals required, anaesthetized animals can be studied. It is not possible to use inhalation anaesthetics as these inhibit brown fat activity Ohlson et al. The anaesthetized animal is placed in a small-volume measuring chamber at a temperature a few degrees higher than thermoneutral 33°C is needed for a mouse , in order to maintain its body temperature Golozoubova et al. After an adequate period of measurement to estimate the basal metabolic rate, the animal is removed and injected with norepinephrine and returned to the chamber. The metabolic rate will rise and plateau Fig. The increase over basal is the nonshivering thermogenic capacity plus the pharmacological response to norepinephrine. Basically, norepinephrine tests can therefore only be used to compare the difference in magnitude of the response between different conditions e. g warm- and cold-acclimated animals ; the absolute magnitude of nonshivering thermogenesis cannot be obtained by this method in itself. It is important to distinguish between adrenergic thermogenesis and nonshivering thermogenesis. is a thermoregulatory thermogenesis. In general, this is probably not the case. It is no surprise that different organs display increased oxygen consumption thermogenesis when stimulated with norepinephrine. In these organs, the cognate metabolic processes are stimulated, and any such stimulation leads to thermogenesis. Thus, norepinephrine stimulation of the salivary gland leads to increased oxygen consumption Terzic and Stoji, , as does stimulation of the liver Binet and Claret, These reactions have never been discussed to represent thermoregulatory thermogenesis; the heat is simply a by-product of the increased metabolism related to increased secretion, etc. Only because muscle is traditionally discussed as being a thermogenic organ are similar adrenergically induced responses in muscle discussed as representing a form of thermoregulatory thermogenesis. Importantly, these brown-fat-independent types of adrenergic thermogenesis have never been shown to be adaptive. This means that they are not recruited during acclimation to cold or adaptation to diet, and they are therefore not part of a thermoregulatory process. Particularly in humans, there are many results from studies using infusions of adrenergic agents and measurements of oxygen consumption Blaak et al. These studies are, for the reasons stated above, probably not relevant for the type of thermogenesis discussed here, i. thermoregulatory nonshivering thermogenesis or diet-induced thermogenesis. To our knowledge, there are no indications that this thermogenesis is adaptive. Additionally, there is the problem that the adrenergic concentrations achieved during infusion, particularly in humans, may be so low that only a hormonal action of adrenergic agonists is induced; i. the levels may not be high enough to reach the postsynaptic areas in a sufficiently high concentration. In that case, brown adipose tissue may not be stimulated at all. The problem with the pharmacological response to norepinephrine can to some extent be overcome by using a specific β 3 -adrenergic agonist, notably CL, As β 3 -adrenergic receptors are only found in high density in adipose tissues, and as white adipose tissue is nearly inert with respect to oxygen consumption, the response seen would mainly emanate from brown adipose tissue, i. However, the response may not represent the true capacity of brown adipose tissue because β 3 - and β 1 -adrenoreceptors may be needed to elicit the total β-adrenergic response, and there may be an α-adrenergic component Mohell et al. Thus, only with norepinephrine is it certain that the entire thermogenic response is induced. Metabolic chambers measure the rate of oxygen consumption, and the outcome is thus in litres of oxygen per unit time. This is an approximation of the total heat production but, because the thermal equivalent of an oxygen molecule is different when carbohydrate or fat is combusted, conversion factors depending on the respiratory quotient should be used to convert the oxygen consumption values to energy W. This is particularly important if the food composition is changed from carbohydrate to fat or during day-and-night measurements when the animals change from burning a mixed diet active phase to burning stored fat inactive phase. The problems occurring by expressing metabolism per kg body weight. The animals symbolized have similar amounts of normal tissue black but different amounts of white adipose tissue grey. Thus, to express metabolic rates per body weight or to any power of body weight leads to misleading conclusions. In studies of all types of metabolism, there is one major difficulty in interpretation and representation of the results: the denominator or the divisor, i. how the results should be expressed. If the animals are of the same size and body composition, there is no problem, but very often this is not the case. It may initially seem natural to express metabolism per gram body weight; however, in reality, animals are often studied that have become obese, e. due to a diet intervention or a genetic alteration. Such animals may have identical amounts of active lean tissue but are carrying expanded amounts of lipid around in their white adipose tissue Fig. Lipid as a chemical is totally metabolically inert, and in no way contributes to metabolism. However, if the metabolic rate is expressed per gram body weight, and one animal carries extra weight in the form of lipid, the metabolic rate expressed in this way will appear smaller in the obese animal. This is evidently not an adequate description. By contrast, if a treatment leads to leanness, the lipid carried around is less, the divisor is smaller and thus we have an explanation for leanness: enhanced thermogenesis Fig. Although these considerations would seem banal, the literature overflows with results calculated this way and conclusions based on these results. The problem has been repeatedly addressed, but still seems to persist Himms-Hagen, ; Butler and Kozak, In an apparently more advanced way, metabolic rates and thermogenic capacities can be expressed per gram body weight raised to some power. Most often the conversion is to grams raised to the power 0. Firstly, evidently this in no way eliminates the problem discussed above; lipid is still inert even if raised to any power. Secondly, the power 0. mice and elephants. It turns out that the metabolism increases in proportion to the body weight to the power 0. For mathematical reasons, the power raising makes nearly no difference if, for example, mice with only somewhat different body weights are compared, and it should therefore only be used for comparisons between species. Occasionally, the power 0. This is the geometrical relationship between the surface area and the volume weight of a sphere or cube. The power relationship is of significance if thermal balance is discussed — but to use it to express rates of metabolism implies that all metabolism is due to heat loss to the surroundings, which is of course not the case. The difference between the powers 0. What, then, is the solution to the dilemma of the divisor? The easiest — and in most circumstances most correct — solution is simply to give the results as per animal. A more sophisticated, and on occasion advantageous, solution is to express the rate per gram lean body mass. Even to express the metabolic rates per gram lean mass assumes that all lean mass in the body has an equal metabolic rate. This is not the case; therefore, although lean mass is a better approximation, it is not without its own problems. After all, if the modification studied should be causative of the development of obesity or protection against obesity , the altered metabolic rate should be present before the new phenotype becomes evident. Brown adipose tissue is an admirable defence mechanism against cold. It has an impressively high oxidative capacity and thermogenic activity per gram of tissue and provides chronically cold-exposed mammals with a comfortable means of defending body temperature. As pointed out above, in its absence, shivering will function but shivering is notably less comfortable than nonshivering thermogenesis and will impose restrictions on the animal's freedom of movement. Some 30 years ago, it was observed that a nonshivering thermogenic capacity could also be recruited by exposing rodents to so-called cafeteria diets or, later, to high-fat diets Rothwell and Stock, The mechanism of recruitment of brown adipose tissue under these conditions has not been clarified but it presumably involves activation of the sympathetic nervous system either directly by components in the diet as has been the general view or secondarily to the developing obesity as such. It was proposed that animals that could develop brown adipose tissue in this way could use its thermogenic capacity to combust excess energy in the diet and thus not become as obese as otherwise expected. Extensive studies by many groups have supported this view Cannon and Nedergaard, but see Maxwell et al. The magnitude of the increase in metabolic rate induced by injected norepinephrine is enhanced following dietary treatment, in a manner similar to that following cold acclimation i. classical nonshivering thermogenesis Rothwell and Stock, ; Feldmann et al. The increases seen are smaller, but it would seem to be an adaptive process, as is classical nonshivering thermogenesis. Also note that this metabolic increase is in addition to that caused by the direct metabolic costs of digesting the food. Whereas the purpose of classical nonshivering thermogenesis is clear, that of diet-induced thermogenesis is not equally evident. There are indications that the magnitude of diet-induced thermogenesis is related to the protein content of the diet. An adequate explanation for the development of diet-induced thermogenesis was proposed by Stock: if diets with inadequate protein or another essential nutrient content — i. unbalanced diets — were eaten to the extent that sufficient protein was ingested, a system had to exist to remove the excess of energy that this extra ingestion had incurred Stock, This system would thus be brown adipose tissue. Good experimental evidence for this hypothesis is still lacking. If an animal does use brown fat thermogenesis to regulate its amount of stored body fat, it would be reasonable to assume that in the absence of active brown fat such as in an animal lacking UCP1 , the animal would become obese, provided it maintained the same energy intake. It was therefore initially surprising perhaps even disappointing that the UCP1-ablated mice did not develop obesity Enerbäck et al. However, later studies performed in mice housed at their thermoneutral temperature showed a development of obesity even on a regular chow diet, and to a greater extent on a high-fat diet Feldmann et al. This indicates that even the very small amount of UCP1 present in the wild-type mice at thermoneutrality is actually effective in modulating body fat content, its absence is not compensated by other means, and the absence is sufficient for obesity to occur. Animals living at their thermoneutral temperatures are not under any cold stress and, therefore, clearly do not have UCP1 and brown fat for this reason. Brown fat is classically recruited in parallel with decreasing ambient temperatures. The presence of some active brown fat even at thermoneutrality can be taken to indicate that it indeed has a physiological function. Surprisingly, mice without UCP1 are protected against diet-obesity when studied under normal animal house conditions. The reason for this is still not clarified but this is not a unique outcome for UCP1-ablated mice. Even mice with UCP1 i. wild-type mice are protected against obesity if they are placed in a cold environment; however, the degree of cold needed for this protection is higher for wild-type than for UCP1-ablated mice Cannon and Nedergaard, Perhaps the most important reason to acquire a thermal understanding when approaching studies of metabolism is to not be misled by false positive observations and thus to invest scientific time and effort in metabolic phenomena that are secondary to thermal regulation rather than to truly altered metabolism. The risk of false positives. If, for example, a mutant mouse has fur with a decreased insulation, the slope of the thermal control curve becomes higher. If this mouse is only maintained and examined at normal temperature here 24°C , it will display a higher metabolism a than the control. The mutant thus appears to be hypermetabolic. In reality, it feels much colder than the wild-type mouse, i. it feels like the wild-type mouse would feel if it were shifted to a lower temperature where the same metabolism would be needed b ; that is it feels as if it were at 14°C c. It will therefore display all the features expected of mice at 14°C, e. All of these effects are, however, secondary to the animal feeling colder and will disappear if the mouse is kept and examined at thermoneutrality. Such examinations are rarely performed. As seen, the mouse of interest for thermoregulatory reasons necessarily shows an increased metabolism a thermogenesis , which wrongly suggests that it has an enhanced metabolism due to some metabolic pathway being modified. the appearance of UCP1-containing cells in white adipose tissue depots Xue et al. All of these observations would undoubtedly be formally correct, but when the thermoregulatory responses of the mouse are examined, these results become trivial in the sense that they are all consequences of decreased insulation. Thus, as indicated in Fig. In this example, all differences would thus be ascribable to the expected effects of feeling colder. The fact that this is more than a theoretical situation has been demonstrated several times recently. For example, a mouse without the fatty acid elongase Elovl3 demonstrated the above characteristics and was experimentally shown to have decreased insulation Westerberg et al. Similarly, the global absence of stearoyl CoA dehydrogenase 1 SCD1 leads to this type of apparently hypermetabolic phenotype Ntambi et al. Thus, the metabolic changes can be explained by the altered skin phenotype, the resultant increased heat loss and the effects of this resultant increased metabolism. The risk of false negatives. If a mutant animal truly has a decreased intrinsic metabolic rate but unchanged body temperature and insulation, it will not display a metabolic rate different from the wild type if kept and examined at normal temperatures a. Only if examined so as to establish the thermoneutral zone of the animal will the decreased metabolism become evident b. This is the case for thyroid receptor null mutants Golozoubova et al. It is likely that many mutants or treatments with true effects on intrinsic metabolism have been overlooked because they have only been examined under conditions where their metabolic rate is controlled by the ambient temperature. Other genetically modified mice have also been shown to exhibit changes in fur and skin properties together with resistance to diet-induced obesity; these include the global knock-out of acyl coenzyme A:diacylglycerol acyltransferase 1 DGAT1 Smith et al. Again, it is unlikely that these modifications truly affect intrinsic metabolism; rather, the outcome is due to thermoregulatory thermogenesis. In addition, mice that lack the thyroid hormone receptor α show an increased metabolism, etc. at 22°C but not at thermoneutrality Marrif et al. The most probable explanation for this is again an insulation problem although the authors propose another mechanism. It is likely that a number of recently published metabolic phenotypes where, for example, activation of brite adipose tissue has been demonstrated may in reality be due to alterations in insulation.

Thermogenesis is genegation process of heat production in hea. It occurs Thermogenesis and body heat generation all het animals, and also in generration few Thermogenesis and body heat generation of thermogenic plants such Thwrmogenesis the Eastern Metabolism and metabolic disorders cabbagethe Voodoo lily Sauromatum venosumand the giant water lilies of the genus Victoria. The lodgepole pine dwarf mistletoe, Arceuthobium americanumdisperses its seeds explosively through thermogenesis. Depending on whether or not they are initiated through locomotion and intentional movement of the musclesthermogenic processes can be classified as one of the following:. One method to raise temperature is through shivering.

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