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The plant is also used traditionally in veterinary practice 2. Coleus forskohlii is the only known natural source of the unique adenylate cyclase activating phytonutrient, forskolin 3.

Adenylate cyclase is the enzyme involved in the production of Cyclic Adenosine Monophosphate cAMP , a significant biochemical agent in metabolic processes.

In many hormone sensitive systems the hormone itself does not enter the target cell but binds to a receptor and indirectly affects the production of another molecule within the cell which then diffuses intracellularly to the target enzymes or a receptor inside the cell to produce the response.

This intracellular mediator is called the second messenger. A recently patented application includes the potentiation of lean body mass and benefits in the management of mood disorders 4.

Potential topical applications include its role as a skin-conditioning agent to support localized fat loss on topical application 5. Research carried out over the last few decades has revealed the multi-faceted pharmacological effects of forskolin.

Most of these effects have been linked to the role of forskolin as an activator of adenylate cyclase 7. Adenylate cyclase is also involved in the regulation of lipolysis or enzymatic breakdown of fat in the adipocytes fat cells. Hormone sensitive lipase mediates lipolysis and this enzyme is activated through phosphorylation by protein kinase A that in turn is activated by cAMP.

Topical fat reduction in specific areas of the body is a common concern for women. Groups of fat cells are attached to the underside of the dermis by fibrous connective tissue.

As fat cells enlarge, the fibers are stretched and pull down on the underlying skin. This causes the indentation or dimpling of the skin called cellulite.

The adrenoreceptors play important roles in the regulation of lipolysis. Adrenoreceptors are neurons that are activated by adrenaline epinephrine or similar substances. The relative number of b-2 and a-2 adrenoreceptors on the surface of the fat cells determine the balance of lipolysis in those cells.

Hormones such as estrogen influence the number of a-2 and b-2 adrenergic receptors in the fat cells. Through the effects of estrogen, women more a-2 adrenergic receptors in fat cells in the hip and thigh region The a-2 adrenoreceptors and the adenosine receptors in fat cells stimulate specific proteins [GTP inhibitory binding proteins G i proteins ] that inhibit adenylate cyclase thereby inhibiting lipolysis.

A healthy balance of lipolysis is maintained through the simultaneous action of the b-2receptors that activate specific proteins [GTP binding proteins G s proteins ] which in turn activate adenylate cyclase and thereby cAMP , stimulating lipolysis.

Due to the increased number of a-2 adrenergic receptors in the hip and thigh region in women, fat mobilizaton becomes more difficult from these areas 5. b-adrenergic stimulation and aadrenergic inhibition has been reported to increase lipolysis from fat cells It has been demonstrated that adipose tissue metabolism varies from one region of the body to another, for example, in severely obese women losing weight after the jejuno-ileal bypass surgery, fat was seen to be absorbed more slowly in the thigh region than the abdominal region These differences lead to the hypothesis that localized application of agents that trigger lipolysis or fatbreakdown could help in cases of fat accumulation at specific subcutaneous sites 4.

Forskolin accelerates lipolysis through the activation of hormone-sensitive lipase Forskolin bypasses the adrenoreceptors, increasing cAMP levels directly, thereby stimulating lipolysis.

The beneficial effects of forskolin, therefore, do not depend upon the sensitivity of the adrenergic receptors, which can often decreases with age and other physiological factors. Forskolin has also been shown to counteract the decreased response of fat cells to epinephrine, associated with aging.

A clinical study performed in 13 established that regional fat loss from the thigh in obese women could be effected through adrenergic modulation. In this study, twenty eight obese women were placed on a calorie-restricted diet and subjected to one of five topical treatments to one thigh three to five times per week for four weeks: 1 isoproterenol injections; 2 cream containing forskolin, aminophylline, and yohimbine; 3 yohimbine cream; 4 forskolin cream; or 5 aminophylline cream.

The opposite thigh was treated with a placebo injection or cream , serving as the control. The treated thighs lost significantly more girth after treatment both by injection and by cream. Additionally, no adverse reactions were observed that could be attributed to either the cream or the injections.

Forskolin has positive effect against a wide range of conditions such as asthma, glaucoma, hypertension, hair loss, cancer, and obesity [ 51 ]. In traditional Indian systems of medicine, the roots of C. forskohlii are used as a tonic. Other therapeutically relevant properties include anthelmintic action and efficacy in the management of skin infections and eruptions.

The plant is also used traditionally in veterinary practice Table 1. Essential oil in tubers of this plant has potential uses in food flavoring industry and can be used as an antimicrobial agent and has very attractive and delicate odor with spicy note.

A labdane diterpenoid is considered the active secondary metabolite because of its ability to activate the enzyme adenylyl cyclase Ac thereby increasing the intracellular level of cAMP and leading to various physiological effects [ 52 ].

FSK is shown to exert a 6— fold increase in levels of cAMP. FSK by passes the adrenoreceptors, increasing cAMP levels directly, thereby stimulating lipolysis.

FSK has also been shown to counteract the decreased response of fat cells to epinephrine, associated with aging. FSK also accelerates lipolysis through the activation of hormone-sensitive lipase [ 54 ]. It is primarily via the increased synthesis of cyclic AMP that C.

Forskohlii may exert its medicinal influences on a significant number of common health conditions. High affinity [3H] FSK-binding sites have been mapped autoradiographically in rat brain area such as caudate-putamen, nucleus accumbens, olfactory tubercle, globus pallidus, substantia nigra and the hilus of the area dentata [ 57 ] and exhibit a markedly heterogeneous distribution.

FSK may activate Ac by interacting with two sites, one which may be directly located on the cyclase molecule, and the other which is associated with OJ somehow formed by the interactions with the N, protein.

FSK, a commonly used activator of Ac [ 55 ], elevates the stimulation-induced release of several transmitters, such as acetylcholine, noradrenaline and 5-hydrdoxytryptamine, from brain or synaptosomes and markedly increasing the rate of conversion of ATP to cyclic AMP [ 58 ].

cAMP could increase the apparent number of Na, K-ATPase sites by either direct or indirect mechanisms. FSK elevates electrically evoked acetylcholine release in the hippocampus independently of Ac activation [ 58 ]. FSK appears to provide a new clue for elucidating the physiological role of cAMP in the synaptic transmission in the sympathetic ganglia.

FSK exerts two opposite pharmacological actions at the synapse, i. a facilitation of transmitter release at the presynaptic site and a depressant action on nicotinic acetylcholine receptor at the postsynaptic site.

FSK reduced the amplitude shock stimulation of preganglionic nerve. FSK induces a reversible AChR desensitization at the junctional and extrajunctional regions in rat [ 59 ].

FSK, an activator of Ac, could increase transmitter release presynaptically in CA1 neurons. FSK directly stimulates Ac and thereby increases cyclic AMP activity, which is known to influence neurite outgrowth and membrane trafficking in neurons.

Increased cyclic AMP activity may have multiple effects on cells including changing the direction of growing neurites [ 60 ] and increasing the density of clathrin-coated pits and coated vesicles at plasma membranes coincident with an increased synthesis of clathrin light chain.

The cAMP effector system enhanced by FSK is involved in the release of dopamine from dopaminergic nerve endings in the neostriatum [ 61 ].

FSK increased dopamine formation in rat striatal slices, rat striatal synaptosomes, rat hypothalamic synaptosomes and bovine retinal slices [ 62 ].

An increase in intracellular cAMP levels through FSK to play an important role in modulating the cytokine production. Intracellular cAMP has been reported to depress the accumulation of tumor necrosis factor TNF-α an mRNA by inhibiting the transcriptional processes.

Elevation of intracellular cAMP levels induced by PDE inhibitors, FSK, prostaglandin E2, or cell-permeable cAMP analogue also inhibited the secretion of IL-1b, whereas it increased IL-1b mRNA levels from lipopolysaccharide-stimulated human monocytes.

Although the regulatory modality of IL-8 production by cAMP is still unclear and depends on the cell type, enhanced cAMP appears to have favorable effects at least on airway cells by suppressing IL-8 production [ 63 ].

Therefore, enhanced cAMP levels by have also FSK been recognized to reverse the increased pulmonary microvascular permeability associated with ischemia reperfusion Figure 4 [ 64 ]. Oxidative stress may play a role in the development and clinical manifestations of autism.

Both central and peripheral markers of oxidative stress have been reported in autism. Peripheral markers have included lipid peroxidation levels. Increases in these markers correlated with loss of previously acquired language skills in autism.

Furthermore, metabolic markers of oxidative stress have been identified including abnormal levels of metabolites signifying impaired methylation and increased oxidative stress in autism [ 65 ]. The oxidative stress in autism may be caused by an imbalance between the generation of ROS and the defense mechanism against ROS by antioxidants.

An increase in reactive oxygen species ROS results in damage to proteins, DNA, and lipids. Specifically, the interaction between ROS and nitric oxide NO results in the nitration of tyrosine residues in proteins and can alter protein conformation and function [ 66 ]. Reactive oxygen species including superoxide O2.

The brain is strongly dependent on the ATP production of the cell energy-producing organelle, the mitochondrion. There is a large body of evidence involving mitochondrial dysfunctions in ASD. Palmieri and Persico, regarding ASD, oxidative phosphorylation OXPHOS in the mitochondrion requires at least 80 proteins, of which only 13 are encoded by the mtDNA, while mitochondrial functioning has been estimated to need the participation of approximately nuclear genes.

Mitochondrial dysfunction is present in the brains of individuals with ASD and may play a role in its core cognitive and behavioral symptoms. Alternatively, mitochondria can be damaged by endogenous stressors associated with ASD such as elevated pro-inflammatory cytokines resulting from an activated immune system or other conditions associated with oxidative stress.

Oxidative stress may be a key link between mitochondrial dysfunction and ASD as reactive oxygen species ROS generated from pro-oxidant environmental toxicants and activated immune cells can result in mitochondrial dysfunction. Excess production of free radicals or impaired antioxidant mechanisms may cause oxidative stress: impaired mitochondrial function then leads to further oxidative stress and a vicious negative cycle can ensue.

Mitochondrial dysfunctioning caused depletion of ATP, that further decrease the level of cAMP. Forskolin, increase in intracellular cAMP, through the phosphorylation of CREB which perform neuroprotective functioning associate with mitochondrial dysfunctioning [ 69 ].

Autistic brain which may reflect enhanced cortical plasticity which is defined as the process of microstructural construction of synapses occurring during development and the remodeling of these synapses during learning [ 70 ]. Enhanced synaptic plasticity triggers a regional reorganization of brain functions that account for both the unique aspects of autism and its variability [ 71 ].

Moreover, on other side FSK act as a co-activator in brain that follows the G S pathway through the activation of D1 receptor. There is least availability of selective AC activation and so far only limited reports suggest beneficial effect of FSK in neurodegeneration animal model.

In conclusion, the current study strongly confirms that the administration of propionic acid induces brain lesions that are similar to the behavioral, histological, morphological, biochemical, neurochemical, and pathological features of autism.

After Chronic administration of propionic acid in the rats as proven by motor dysfunctions, biochemical and neurochemical alternations. Thus in conclusion, neuroprotective and neuro restoration effects of FSK may be due to favorable modulation of CREB-mediated signaling. So, now we can finally conclude the significant mitochondrial restorative effects of the FSK may be due to showing its improved motor and cognitive functions as well as to restore the energy levels and antioxidant and anti-inflammatory defense system.

The authors express their gratitude to Chairman, Mr. Parveen Garg, and Director, Dr. Gupta, ISF College of Pharmacy, Moga Punjab , India, for their great vision and support. Authors are really thankful to Dr.

Vikramdeep Monga, for valuable support and encouragement. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Edited by Antonella Borreca. DOWNLOAD FOR FREE Share Cite Cite this chapter There are two ways to cite this chapter:. Choose citation style Select style Vancouver APA Harvard IEEE MLA Chicago Copy to clipboard Get citation.

Choose citation style Select format Bibtex RIS Download citation. IntechOpen Recent Advances in Neurodegeneration Edited by Antonella Borreca. From the Edited Volume Recent Advances in Neurodegeneration Edited by Antonella Borreca Book Details Order Print.

Chapter metrics overview 1, Chapter Downloads View Full Metrics. Impact of this chapter. Abstract New developments in the study of brain are among the most exciting frontiers of contemporary neuroscientific research for the clinical practitioner. Keywords neurodegeneration autism mitochondrial dysfunction adenylyl cyclase forskolin.

mehan gmail. Introduction Neurological disorders are a heterogeneous group of diseases of the nervous system having different etiologies. Propionic acid and autism Propionic acid PPA is a short chain fatty acid formed endogenously in the human body as an intermediate of fatty acid metabolism and a metabolic end product of enteric gut micro biota such as clostridia and propionic bacteria [ 43 , 44 , 45 , 46 ].

Pharmacological activity Mechanism of action Ref. Anti-depressant FSK stimulated AC activity in rat brain and leads to enhancement of the coupling between stimulatory GTP-binding protein G protein and AC catalytic molecules FSK stimulates AC and regulates brain-derived neurotrophic factor BDNF and TrkB expression in the rat brain 92 ii.

Anti-cancer Restoration of PP2A activity with forskolin that inhibit Akt and ERK activity and block proliferation and induce caspase-dependent apoptosis in AML cell lines. Antispasmodic activity increase of cAMP inhibit cramping or smooth muscle contraction 95 v.

Anti-Glaucoma Stimulates Adenylate cyclase which stimulates the ciliary epithelium to produce cyclic adenosine monophosphate cAMP that results in decreased aqueous humor inflow there by decrease in IOP Reduction of intra ocular pressure 96 vi. Cardioprotective amelioration of Mitochondrial dysfunction in cardiomyopathy It reduces diastolic blood pressure without increasing myocardial oxygen consumption.

Anti-asthmatic Forskolin activation of cAMP inhibits human basophil and mast cell degranulation, resulting in subsequent bronchodilation 98 viii. Anti-psoriasis Decreased cGMP levels that are associated with cell proliferation and thus decrease cell division.

Hepatoprotective activity Repair of hepatic tissue damage, normalization of inflammatory hepatic and necrosis Forskolin increases cAMP accumulation, and therefore stimulates lipolysis. Anti-inflammatory Reduction in the level of Interleukin-1β, 6 and 8 Overexpression of TANK-binding kinase 1 TBK1 reduced phosphorylation of hormone-sensitive lipase HSL in response to FSK Inhibit mast cell degranulation xi.

Anti-diabetic activity FSK predominantly decreased basal glucose in healthy rats and attenuated the severity of hyperglycemia in diabetic rats FSK increase intracellular cAMP, which, together with the increase in ATP, enhance the priming of insulin granules xii.

Anti-platelet aggregation Antagonizes the action of platelet-activating factor PAF. Reduction in the extent of platelet aggregation Induced a partial deaggregation of ADP- or collagen-aggregated human platelets xiii. Inhibition of human neutrophil degranulation Anti-histaminic activity cAMP-mediated phosphodiesterase inhibition.

Reduction in the histamine release from human basophiles and mast cells by modulating the release of mediators of the immediate hypersensitivity reaction, through activation of AC xiv.

Hydrodynamic alterations in collecting tubule Anti-cystic fibrosis FSK resulted in increase in osmotic water flux and hydraulic conductivity of the rabbit cortical collecting tubule FSK leads to cyst formation in culture media Table 1.

Pharmacological action of FSK. FSK-binding sites 3H-forskolin has, for example, been found to bind to both a high and a low affinity site in rat brain membranes [ 55 ] and the capacity of the high affinity forskolin-binding site has been shown to be increased by the activation of N-proteins by guanine nucleotides [ 56 ].

Role of FSK in brain FSK may activate Ac by interacting with two sites, one which may be directly located on the cyclase molecule, and the other which is associated with OJ somehow formed by the interactions with the N, protein.

FSK against neuroinflammation An increase in intracellular cAMP levels through FSK to play an important role in modulating the cytokine production. Forskolin against neurooxidation Oxidative stress may play a role in the development and clinical manifestations of autism.

Forskolin against mitochondrial dysfunctioning The brain is strongly dependent on the ATP production of the cell energy-producing organelle, the mitochondrion. Forskolin against cognitive dysfunction Autistic brain which may reflect enhanced cortical plasticity which is defined as the process of microstructural construction of synapses occurring during development and the remodeling of these synapses during learning [ 70 ].

References 1. Swerdlow RH. Mitochondrial DNA—related mitochondrial dysfunction in neurodegenerative diseases. Kermer P, Liman J, Jochen H. Neuronal apoptosis in neurodegenerative diseases: From basic research to clinical application.

Neurodegenerative Diseases. Song JH, Huang CS, Nagata K, Yeh JZ, Narahash T. Differential action of riluzole on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels.

Journal of Pharmacology and Experimental Therapeutics. Chalasani SH, Sabelko KA, Sunshine MJ. A chemokine, SDF-1, reduces the effectiveness of multiple axonal repellents and is required for normal axon pathfinding.

The Journal of Neuroscience. Shewan D, Dwivedy A, Anderson R, Holt CE. Age-related changes underlie switch in netrin-1 responsiveness as growth cones advance along visual pathway. Nature Neuroscience. Akassoglou K. Nerve growth factor-independent neuronal survival: A role for NO donors.

Molecular Pharmacology. Cai D, Qiu J, Cao Z. Neuronal cyclic AMP controls the developmental loss in ability of axons to regenerate. Frey U, Huang YY, Kandel ER. Effects of cAMP simulates a late stage of LTP in hippocampal CA1 neurons. Marx G. The Molecular Basis of Memory. Secure transaction Your transaction is secure.

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Search this page. Purchase options and add-ons. Brand Natures Craft Flavor Unflavored Primary Supplement Type Forskolin Unit Count 60 Count Item Form Capsule Item Weight 2 Ounces Item Dimensions LxWxH 1. About this item Pure forskolin pills - Experience healthy weight loss by using our forskolin supplement for men and women.

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Learn more how customers reviews work on Amazon. Customers say. Quality Appetite Weight loss Energy Value Ease of use Blood pressure Effect on skin. Images in this review. Reviews with images. See all photos. All photos. That it works and lasts a long time. I had heard about Forskolin for quite a while and had been trying to lose weight forever and nothing was working so I decided to try Forskolin.

So I ordered a bottle, very expensive I thought but I was desperate and tried it and in 2 months went from pounds to pounds and still losing a little bit at a time. I am not following a diet and because I have a knee in need of replacing and a very bad back I cannot exercise, yet losing weight in spite of this.

Forskolin and I will be losing even more weight. I can't wait to get my knee fixed and be able to walk again so I can add walking back in my life and lose even more weight. And I am looking more attractive every pound lost.

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Journal of the Ahd Forskolin and mood enhancement Forrskolin Sports Nutrition enhaancement 2Article number: 54 OFrskolin this article. Metrics details. This enhancemeny investigated Digestive enzyme supplements effects of Coleus Forskohlii CF on body composition, and determined the safety and efficacy of supplementation. Fasting blood samples and dietary records 4-d were obtained at 0 and wks. Side effects were recorded on a weekly basis. Data were analyzed by repeated measures ANOVA and are presented as mean changes from baseline for the CF and placebo groups, respectively. No significant differences were observed in caloric or macronutrient intake.

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Proven Supplements to Increase Testosterone Ft. Andrew Huberman Eenhancement also Potassium and weight management the popular Forskolin and mood enhancement Expert YouTube enhahcement. Forskolin Coleus forskohlii is the only known supplement to naturally boost Forskolin and mood enhancement Cyclic Adenosine Monophosphate in your Forskloin. cAMP is important for neural signaling within brain cells. As a secondary messenger in neuronscAMP produces proteins needed for neuron and synapse growth. This process is called Long-Term Potentiation LTP. LTP is the process where synaptic connections get stronger in response to electrical stimulation in the brain. This process happens naturally through life experience.