They used additional datasets, mathematical models, and adjustments to account for differences in body size, age, and reproductive status.

Their findings revealed four distinct phases of adjusted total and basal energy expenditure over the lifespan. Neonatal 1 month to 1 year : Neonates in the first month of life had size-adjusted energy expenditure similar to that of adults.

Energy expenditure increased rapidly over the first year, reaching a peak at 0. Childhood and adolescence 1 to 20 years : Although total and basal expenditure as well as fat-free mass continued to increase with age throughout childhood and adolescence, size-adjusted expenditures steadily declined throughout this period.

Sex had no effect on the rate of decline. At Of note, there was no increase in adjusted total or basal energy expenditure during the pubertal ages of 10 to 15 years old. Adulthood 20 to 60 years : Total and basal expenditure and fat-free mass were all stable from ages 20 to 60, regardless of sex.

Adjusted TEE and RMR remained stable even during pregnancy, and any increase in unadjusted energy expenditure during pregnancy was accounted for by the increase in body mass. The point at which adjusted TEE started to decline was age 63, and for adjusted BMR was age During this reaction, additional protons are transferred to the intermembrane space.

As the protons flow from the intermembrane space through the ATP synthase complex and into the matrix, ATP is formed from ADP and inorganic phosphate P i in the mitochondrial matrix.

Oxidative phosphorylation depends on the electron transport from NADH or FADH 2 to O 2 , forming H 2 O. The electrons are "transported" through a number of protein complexes located in the inner mitochondrial membrane, which contains attached chemical groups flavins, iron-sulfur groups, heme, and cooper ions capable of accepting or donating one or more electrons Figure 2.

These protein complexes, known as the electron transfer system ETS , allow distribution of the free energy between the reduced coenzymes and the O 2 and more efficient energy conservation. The electrons are transferred from NADH to O 2 through three protein complexes: NADH dehydrogenase, cytochrome reductase, and cytochrome oxidase.

Electron transport between the complexes occurs through other mobile electron carriers, ubiquinone and cytochrome c. FAD is linked to the enzyme succinate dehydrogenase of the TCA cycle and another enzyme, acyl-CoA dehydrogenase of the fatty acid oxidation pathway.

During the reactions catalyzed by these enzymes, FAD is reduced to FADH 2 , whose electrons are then transferred to O 2 through cytochrome reductase and cytochrome oxidase, as described for NADH dehydrogenase electrons Figure 2. These observations led Peter Mitchell, in , to propose his revolutionary chemiosmotic hypothesis.

The reaction catalyzed by succinyl-CoA synthetase in which GTP synthesis occurs is an example of substrate-level phosphorylation. Acetyl-CoA enters the tricarboxylic acid cycle at the top of the diagram and reacts with oxaloacetate and water H 2 O to form a molecule of citrate and CoA-SH in a reaction catalyzed by citrate synthase.

Next, the enzyme aconitase catalyzes the isomerization of citrate to isocitrate. Succinyl-CoA reacts with GDP and inorganic phosphate P i to form succinate and GTP. This reaction releases CoA-SH and is catalyzed by succinyl-CoA synthetase.

In the next step, succinate reacts with FAD to form fumarate and FADH 2 in a reaction catalyzed by succinate dehydrogenase. Fumarate combines with H 2 O in a reaction catalyzed by fumerase to form malate.

Then, oxaloacetate can react with a new molecule of acetyl-CoA and begin the tricarboxylic acid cycle again. The diagram shows the molecular structures for citrate, isocitrate, alpha-ketoglutarate, succinyl-CoA, succinate, fumarate, malate, and oxaloacetate.

The enzymes that act at each of the eight steps in the cycle are shown in yellow rectangles. In aerobic respiration or aerobiosis, all products of nutrients' degradation converge to a central pathway in the metabolism, the TCA cycle. In this pathway, the acetyl group of acetyl-CoA resulting from the catabolism of glucose, fatty acids, and some amino acids is completely oxidized to CO 2 with concomitant reduction of electron transporting coenzymes NADH and FADH 2.

Consisting of eight reactions, the cycle starts with condensing acetyl-CoA and oxaloacetate to generate citrate Figure 3. In addition, a GTP or an ATP molecule is directly formed as an example of substrate-level phosphorylation. In this case, the hydrolysis of the thioester bond of succinyl-CoA with concomitant enzyme phosphorylation is coupled to the transfer of an enzyme-bound phosphate group to GDP or ADP.

Also noteworthy is that TCA cycle intermediates may also be used as the precursors of different biosynthetic processes. The TCA cycle is also known as the Krebs cycle, named after its discoverer, Sir Hans Kreb.

Krebs based his conception of this cycle on four main observations made in the s. The first was the discovery in of the sequence of reactions from succinate to fumarate to malate to oxaloacetate by Albert Szent-Gyorgyi, who showed that these dicarboxylic acids present in animal tissues stimulate O 2 consumption.

The second was the finding of the sequence from citrate to α-ketoglutarate to succinate, in , by Carl Martius and Franz Knoop. Next was the observation by Krebs himself, working on muscle slice cultures, that the addition of tricarboxylic acids even in very low concentrations promoted the oxidation of a much higher amount of pyruvate, suggesting a catalytic effect of these compounds.

And the fourth was Krebs's observation that malonate, an inhibitor of succinate dehydrogenase, completely stopped the oxidation of pyruvate by the addition of tricarboxylic acids and that the addition of oxaloacetate in the medium in this condition generated citrate, which accumulated, thus elegantly showing the cyclic nature of the pathway.

When 1,3-bisphosphoglycerate is converted to 3-phosphoglycerate, substrate-level phosphorylation occurs and ATP is produced from ADP. Then, 3-phosphoglycerate undergoes two reactions to yield phosphoenolpyruvate. Next, phosphoenolpyruvate is converted to pyruvate, which is the final product of glycolysis.

During this reaction, substrate-level phosphorylation occurs and a phosphate is transferred to ADP to form ATP. Interestingly, during the initial phase, energy is consumed because two ATP molecules are used up to activate glucose and fructosephosphate.

Part of the energy derived from the breakdown of the phosphoanhydride bond of ATP is conserved in the formation of phosphate-ester bonds in glucosephosphate and fructose-1,6-biphosphate Figure 4.

In the second part of glycolysis, the majority of the free energy obtained from the oxidation of the aldehyde group of glyceraldehyde 3-phosphate G3P is conserved in the acyl-phosphate group of 1,3- bisphosphoglycerate 1,3-BPG , which contains high free energy. Then, part of the potential energy of 1,3BPG, released during its conversion to 3-phosphoglycerate, is coupled to the phosphorylation of ADP to ATP.

The second reaction where ATP synthesis occurs is the conversion of phosphoenolpyruvate PEP to pyruvate. PEP is a high-energy compound due to its phosphate-ester bond, and therefore the conversion reaction of PEP to pyruvate is coupled with ADP phosphorylation.

This mechanism of ATP synthesis is called substrate-level phosphorylation. For complete oxidation, pyruvate molecules generated in glycolysis are transported to the mitochondrial matrix to be converted into acetyl-CoA in a reaction catalyzed by the multienzyme complex pyruvate dehydrogenase Figure 5.

When Krebs proposed the TCA cycle in , he thought that citrate was synthesized from oxaloacetate and pyruvate or a derivative of it. Only after Lipmann's discovery of coenzyme A in and the subsequent work of R. Stern, S. Ochoa, and F. Lynen did it become clear that the molecule acetyl-CoA donated its acetyl group to oxaloacetate.

Until this time, the TCA cycle was seen as a pathway to carbohydrate oxidation only. Most high school textbooks reflect this period of biochemistry knowledge and do not emphasize how the lipid and amino acid degradation pathways converge on the TCA cycle.

The cell is depicted as a large blue oval. A smaller dark blue oval contained inside the cell represents the mitochondrion.

The mitochondrion has an outer mitochondrial membrane and within this membrane is a folded inner mitochondrial membrane that surrounds the mitochondrial matrix. The entry point for glucose is glycolysis, which occurs in the cytoplasm.

Glycolysis converts glucose to pyruvate and synthesizes ATP. Pyruvate is transported from the cytoplasm into the mitochondrial matrix. Pyruvate is converted to acetyl-CoA, which enters the tricarboxylic acid TCA cycle.

In the TCA cycle, acetyl-CoA reacts with oxaloacetate and is converted to citrate, which is then converted to isocitrate. Isocitrate is then converted to alpha-ketoglutarate with the release of CO 2.

Then, alpha-ketoglutarate is converted to succinyl-CoA with the release of CO 2. Succinyl-CoA is converted to succinate, which is converted to fumarate, and then to malate. Malate is converted to oxaloacetate. Then, the oxaloacetate can react with another acetyl-CoA molecule and begin the TCA cycle again.

In the TCA cycle, electrons are transferred to NADH and FADH 2 and transported to the electron transport chain ETC. The ETC is represented by a yellow rectangle along the inner mitochondrial membrane. The ETC results in the synthesis of ATP from ADP and inorganic phosphate P i.

Fatty acids are transported from the cytoplasm to the mitochondrial matrix, where they are converted to acyl-CoA. Acyl-CoA is then converted to acetyl-CoA in beta-oxidation reactions that release electrons that are carried by NADH and FADH 2.

These electrons are transported to the electron transport chain ETC where ATP is synthesized. Amino acids are transported from the cytoplasm to the mitochondrial matrix.

Then, the amino acids are broken down in transamination and deamination reactions. The products of these reactions include: pyruvate, acetyl-CoA, oxaloacetate, fumarate, alpha-ketoglutarate, and succinyl-CoA, which enter at specific points during the TCA cycle.

This pathway is known as β-oxidation because the β-carbon atom is oxidized prior to when the bond between carbons β and α is cleaved Figure 6. The four steps of β-oxidation are continuously repeated until the acyl-CoA is entirely oxidized to acetyl-CoA, which then enters the TCA cycle.

In the s, a series of experiments verified that the carbon atoms of fatty acids were the same ones that appeared in the acids of TCA cycle. Holmes, F. Lavoisier and the Chemistry of Life. Madison: University of Wisconsin Press, Krebs, H.

Nobel Prize Lecture org, Kresge, N. Our bodies need this energy to do everything from moving to thinking to growing. Specific proteins in the body control the chemical reactions of metabolism. Thousands of metabolic reactions happen at the same time — all regulated by the body — to keep our cells healthy and working.

After we eat food, the digestive system uses enzymes to:. The body can use sugar, amino acids, and fatty acids as energy sources when needed. These compounds are absorbed into the blood, which carries them to the cells. After they enter the cells, other enzymes act to speed up or regulate the chemical reactions involved with "metabolizing" these compounds.

During these processes, the energy from these compounds can be released for use by the body or stored in body tissues, especially the liver, muscles, and body fat.

Anabolism pronounced: uh-NAB-uh-liz-um , or constructive metabolism, is all about building and storing. It supports the growth of new cells, the maintenance of body tissues, and the storage of energy for future use.

In anabolism, small molecules change into larger, more complex molecules of carbohydrates, protein, and fat. Catabolism pronounced: kuh-TAB-uh-liz-um , or destructive metabolism, is the process that produces the energy needed for all activity in the cells.

Cells break down large molecules mostly carbs and fats to release energy. This provides fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. As complex chemical units break down into more simple substances, the body releases the waste products through the skin, kidneys, lungs, and intestines.

Several hormones of the endocrine system help control the rate and direction of metabolism.

Pick up the pace. Add some high-intensity interval training to your regular routine. After a period of interval training, your metabolism can stay revved up for as much as a full day. For example, when you're walking or jogging on a treadmill or outside, speed up for 30 to 60 seconds, and then slow to your usual pace; repeat the cycle for eight to 12 minutes.

Eat protein and do weight training. Your metabolism increases whenever you eat, digest, and store food, a process called thermic effect of food. Protein has a higher thermic effect compared with fats and carbohydrates because it takes longer for your body to burn protein and absorb it.

It's not clear how much of an effect protein has on metabolism, but studies suggest the best approach is to combine adequate protein intake with weight training, which increases muscle mass — and that also can boost metabolism. Drink green tea. Studies have found green tea contains a compound called epigallocatechin gallate, which may increase the calories and fat you burn.

A meta-analysis published in Obesity Reviews found that consuming about milligrams of epigallocatechin gallate the amount in about three cups of green tea helped boost metabolism enough to burn an average of extra calories a day.

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Calories provide the energy the body needs, not only to move but also to breathe, digest food, circulate blood, grow cells, repair wounds, and even to think. The rate at which the body burns calories to produce this energy is called the metabolic rate. Scientists use various formulae to measure resting metabolic rate RMR , also known as resting energy expenditure REE.

RMR and REE refer to the amount of energy a body uses at rest, for example, sleeping or sitting. The rate can vary between individuals.

Factors affecting it include age, sex, and the activity the person is carrying out at the time. While a person has no control over the genetic aspects of their metabolism, research shows that some strategies may help speed up the rate at which the body processes calories.

It is worth noting that, while speeding up the metabolism may help people burn calories and lose weight, it needs to be part of an overall strategy that includes a healthy and varied diet and regular exercise.

The authors also hypothesized that meal timing may play a role in resting energy expenditure. However, the results were not conclusive, and more reseach is needed. Learn about time-restricted eating , which focuses on the timing of meals to improve health and gain muscle. Some people skip meals as a way to lose weight.

However, this can negatively impact metabolism. Eating meals that are not filling can have the same effect. According to current dietary guidelines, adult females aged 19 and over need 1,—2, calories a day, depending on their physical activity levels, and males need 2,—3, During pregnancy and breastfeeding, females will need up to additional calories, depending on the stage.

How many calories should I eat per day? Reducing calories may not increase metabolic rate, but the choice of foods that provide those calories may do. Protein, for example, may be more likely than carbohydrates or fat to promote thermogenesis, the burning of calories in the body.

Those who consumed a higher proportion of protein burned more energy than those who consumed less. Some research has suggested that green tea extract may play a role in promoting fat metabolism.

While the Academy of Nutrition and Dietetics says any increase is likely to be small, green tea may help manage weight and health in other ways. The National Center for Complementary and Integrative Health says it is safe to consume up to 8 cups of green tea a day.

People should speak with a doctor before increasing their intake of green tea or consuming it during pregnancy. It may interact with some medications. During pregnancy, it may increase the risk of birth defects due to low folic acid levels.

Does green tea help with weight loss? The authors of a small study found that combining resistance training with dietary measures led to a slight increase in metabolic rate, but it was not statistically significant.

Participants who did only resistance training saw a reduction in fat mass and an increase in lean mass. Research suggests that when a person has more muscle mass, their body uses food for energy more effectively. In other words, their metabolism is less wasteful.

The researchers suggested that fat free mass lean mass and thyroid hormone levels might help account for the variability. Resistance training may involve lifting weights and doing exercises that use the weight of the body or resistance bands to build muscle.

A previous study , from , found that high intensity interval resistance training also increased metabolic rate. Interval training is highly intensive and may be more suitable for people who are already fit than those who are new to regular exercise.

How can exercise help you build muscle? Staying hydrated is essential for the body to function at its best. Water is necessary for optimal metabolism, and it may help a person lose weight. In , scientists assessed the metabolic rate of 13 people who consumed either or milliliters ml of water.

They found evidence of increased fat oxidation after ml when a person is at rest, and concluded that drinking water may have an impact on metabolism. However, they did not find that it increased metabolic rate. This may happen because the additional water helps the body burn fat preferentially over carbohydrate.

How much water should I drink each day? Stress affects hormone levels, and it can cause the body to produce more cortisol than usual.

Cortisol is a hormone that helps regulate appetite. In , researchers found unusually high cortisol levels in people with disordered eating. The body releases cortisol in times of stress.

However, the authors of a small study found no evidence linking resting metabolic rate and anxiety. Stress could also have an indirect impact by affecting eating patterns and sleep, both of which can alter the rate of metabolism.

Why does stress happen, and how can I manage it? People who have less sleep may have a lower metabolic rate, according to research from The study took place in a sleep laboratory, and participants slept 4 hours per night for 5 nights followed by one night of 12 hours sleep.

Their metabolic rate fell after the nights with little sleep but returned to their usual levels after the night of recovery sleep. The authors believed the body reduces metabolic rate to conserve energy when a person sleeps less. They noted this could lead to weight gain in people who do not get enough sleep.

The need for sleep varies between individuals, but the Centers for Disease Control and Prevention CDC recommend that adults aged 18—60 should have at least 7 hours per night. What should you do if you have trouble sleeping? The results of a rodent experiment from suggested that a low intake of various B vitamins could impact the rate at which the body metabolizes lipids, including cholesterol and triglycerides.

More research may be needed to understand the relationship between vitamins, metabolism, and weight loss. A complete guide to B vitamins, types, sources, and more. Some research has suggested that eating spices such as chili, which contains capsaicin, can increase metabolic rate, including the rate at which the body burns fat and uses energy.

A study from China found that people who ate spicy food every day were more likely to have a high body mass index BMI than those who did not. The researchers noted that more investigations are needed to find out why this happens.

The Academy of Nutrition and Dietetics says that while eating hot chilies might boost metabolic rate temporarily, it is unlikely to have a significant impact.

Molecular Cell Biology. Brock Mikrobiologie Aufl ed. München: Pearson Studium. Energy : production, conversion, storage, conservation, and coupling Second ed.

Lincoln: Springer. Microbiological Reviews. Applied Microbiology and Biotechnology. British Journal of Nursing. Journal of Parenteral and Enteral Nutrition. Current Opinion in Cell Biology. A new pH-based etiopathogenic perspective and therapeutic approach to an old cancer question". Critical Reviews in Biochemistry and Molecular Biology.

The Journal of Nutrition. Annual Review of Biophysics and Biomolecular Structure. Archived PDF from the original on 22 January Retrieved 11 November Trends in Biochemical Sciences. Annual Review of Microbiology.

Archived from the original on 2 May Retrieved 6 October December FEMS Microbiology Reviews. Journal of Experimental Botany. July Applied and Environmental Microbiology. Bibcode : ApEnM.. Journal of Bacteriology. Retrieved 3 July FEBS Letters.

Bibcode : Natur. Retrieved 4 July FASEB Journal. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences.

Bibcode : RSPTB. From metabolites to molecular genetics". Diabetes Care. Molecular Microbiology. Surgery Oxford. Archived from the original on 31 October Retrieved 28 August In Varki A, Cummings RD, Esko JD, Stanley P eds.

Essentials of Glycobiology 3rd ed. Cold Spring Harbor NY : Cold Spring Harbor Laboratory Press. Archived from the original on 24 February Retrieved 8 July Molecular Membrane Biology. Annual Review of Plant Physiology and Plant Molecular Biology. Journal of Biosciences. Archived from the original PDF on 15 April Natural Product Reports.

Nucleic Acids Research. Textbook of Medical Physiology. Philadelphia: Elsevier. Archived from the original on 1 May Bacteriological Reviews. Zrenner R, Stitt M, Sonnewald U, Boldt R Annual Review of Plant Biology.

Journal of Plant Physiology. BMB Reports. Archived PDF from the original on 24 October Retrieved 18 September Current Opinion in Structural Biology. Principles and overview". Current Drug Metabolism. Trends in Biotechnology. Environmental Microbiology. Bibcode : EnvMi Archived PDF from the original on 11 November Biochemical Society Symposium.

The Journal of Cell Biology. Experimental Physiology. Current Pharmaceutical Design. Thermodynamic analysis of microbial growth". Biochimica et Biophysica Acta BBA - Bioenergetics.

Biophysical Chemistry. Archived from the original on 4 August Retrieved 22 September Journal of Cell Science. Bibcode : q. The Journal of Experimental Biology. Archived from the original on 29 March Retrieved 12 March Journal of Theoretical Biology. Bibcode : JThBi. Essays in Biochemistry.

Bioscience Reports. Quarterly Reviews of Biophysics. Scientific American. Bibcode : SciAm. Current Molecular Medicine. Archived PDF from the original on 19 June Retrieved 25 March Research in Microbiology.

How Did Bacteria Come to Be? BMC Bioinformatics. Alves R, Chaleil RA, Sternberg MJ July Journal of Molecular Biology. Wernegreen JJ December The Proceedings of the Nutrition Society.

and why are they there? Current Opinion in Plant Biology. Current Opinion in Biotechnology. February CiteSeerX Retrieved 29 December Metabolic Engineering. hdl : October Annual Review of Biomedical Engineering.

Archived from the original on 21 September Retrieved 23 July The Lagoon: How Aristotle Invented Science. Ibn Al-Nafis as a philosopher.

Symposium on Ibn al-Nafis, Second International Conference on Islamic Medicine. Kuwait: Islamic Medical Organization. American Journal of Nephrology. Modern Development of the Chemical and Biological Sciences.

A History of Science: in Five Volumes. New York: Harper and Brothers. Retrieved 26 March From Friedrich Wöhler to Hans A. Rose S, Mileusnic R The Chemistry of Life. Penguin Press Science. Schneider EC, Sagan D Into the Cool: Energy Flow, Thermodynamics, and Life. University of Chicago Press.

Lane N Oxygen: The Molecule that Made the World. USA: Oxford University Press. Price N, Stevens L Fundamentals of Enzymology: Cell and Molecular Biology of Catalytic Proteins. Oxford University Press. ISBN X. Berg J, Tymoczko J, Stryer L Freeman and Company.

Cox M, Nelson DL Palgrave Macmillan. Brock TD , Madigan MR, Martinko J, Parker J Brock's Biology of Microorganisms. Benjamin Cummings. Da Silva JJ, Williams RJ The Biological Chemistry of the Elements: The Inorganic Chemistry of Life. Clarendon Press. Nicholls DG, Ferguson SJ Academic Press Inc.

Wood HG February Wikiversity has learning resources about Topic:Biochemistry. Wikibooks has more on the topic of: Metabolism. Look up metabolism in Wiktionary, the free dictionary. Wikimedia Commons has media related to Metabolism.

Articles related to Metabolism. Metabolism map. Carbon fixation. Photo- respiration. Pentose phosphate pathway. Citric acid cycle.

Glyoxylate cycle. Urea cycle. Fatty acid synthesis. Fatty acid elongation. Beta oxidation. beta oxidation. Glyco- genolysis.

Glyco- genesis. Glyco- lysis. Gluconeo- genesis. Pyruvate decarb- oxylation. Keto- lysis. Keto- genesis. feeders to gluconeo- genesis.

Light reaction. Oxidative phosphorylation. Amino acid deamination. Citrate shuttle. MVA pathway. MEP pathway. Shikimate pathway. Glycosyl- ation. Sugar acids. Simple sugars. Nucleotide sugars. Propionyl -CoA. Acetyl -CoA. Oxalo- acetate. Succinyl -CoA. α-Keto- glutarate. Ketone bodies. Respiratory chain.

Serine group. Branched-chain amino acids. Aspartate group. Amino acids. Ascorbate vitamin C. Bile pigments. Cobalamins vitamin B Various vitamin Bs. Calciferols vitamin D. Retinoids vitamin A. Nucleic acids. Terpenoid backbones.

Bile acids. Glycero- phospholipids. Fatty acids. Glyco- sphingolipids. Polyunsaturated fatty acids. Endo- cannabinoids. Metabolism , catabolism , anabolism. Metabolic pathway Metabolic network Primary nutritional groups.

Purine metabolism Nucleotide salvage Pyrimidine metabolism Purine nucleotide cycle. Pentose phosphate pathway Fructolysis Polyol pathway Galactolysis Leloir pathway. Glycosylation N-linked O-linked.

Photosynthesis Anoxygenic photosynthesis Chemosynthesis Carbon fixation DeLey-Doudoroff pathway Entner-Doudoroff pathway. Xylose metabolism Radiotrophism. Fatty acid degradation Beta oxidation Fatty acid synthesis. Steroid metabolism Sphingolipid metabolism Eicosanoid metabolism Ketosis Reverse cholesterol transport.

Metal metabolism Iron metabolism Ethanol metabolism Phospagen system ATP-PCr. Fructose-bisphosphate aldolase Aldolase A , B , C Triosephosphate isomerase. Glyceraldehyde 3-phosphate dehydrogenase Phosphoglycerate kinase Phosphoglycerate mutase Enolase Pyruvate kinase PKLR , PKM2. Pyruvate carboxylase Phosphoenolpyruvate carboxykinase.

Lactate dehydrogenase. Alanine transaminase. Glycerol kinase Glycerol dehydrogenase. Fructose 6-P,2-kinase:fructose 2,6-bisphosphatase PFKFB1 , PFKFB2 , PFKFB3 , PFKFB4 Bisphosphoglycerate mutase.

Metabolism : carbohydrate metabolism fructose and galactose enzymes. Hepatic fructokinase Aldolase B Triokinase.

Sorbitol dehydrogenase Aldose reductase. Lactose synthase Lactase. Mannose phosphate isomerase. Metabolism : carbohydrate metabolism proteoglycan enzymes.

L-xylulose reductase L-gulonolactone oxidase UDP-glucuronate 5'-epimerase Xylosyltransferase Sulfotransferase Heparan sulfate EXT1 EXT2 Chondroitin sulfate PAPSS1 PAPSS2.

Iduronatesulfatase Iduronidase. Heparan sulfamidase N-acetyltransferase Alpha-N-acetylglucosaminidase Glucuronidase N-acetylglucosaminesulfatase. gov means it's official. Federal government websites often end in. gov or. Before sharing sensitive information, make sure you're on a federal government site.

The site is secure. NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. Cooper GM. The Cell: A Molecular Approach. Sunderland MA : Sinauer Associates; Many tasks that a cell must perform, such as movement and the synthesis of macromolecules, require energy.

A large portion of the cell's activities are therefore devoted to obtaining energy from the environment and using that energy to drive energy-requiring reactions. Although enzymes control the rates of virtually all chemical reactions within cells, the equilibrium position of chemical reactions is not affected by enzymatic catalysis.

The laws of thermodynamics govern chemical equilibria and determine the energetically favorable direction of all chemical reactions. Many of the reactions that must take place within cells are energetically unfavorable, and are therefore able to proceed only at the cost of additional energy input.

Consequently, cells must constantly expend energy derived from the environment. The generation and utilization of metabolic energy is thus fundamental to all of cell biology. The energetics of biochemical reactions are best described in terms of the thermodynamic function called Gibbs free energy G , named for Josiah Willard Gibbs.

The change in free energy Δ G of a reaction combines the effects of changes in enthalpy the heat that is released or absorbed during a chemical reaction and entropy the degree of disorder resulting from a reaction to predict whether or not a reaction is energetically favorable.

For example, consider a hypothetical reaction in which A is converted to B:. The Δ G of a reaction is determined not only by the intrinsic properties of reactants and products, but also by their concentrations and other reaction conditions e. It is thus useful to define the free-energy change of a reaction under standard conditions.

Standard conditions are considered to be a 1- M concentration of all reactants and products, and 1 atm of pressure. The standard free-energy change Δ G ° of a reaction is directly related to its equilibrium position because the actual Δ G is a function of both Δ G° and the concentrations of reactants and products.

For example, consider the reaction. The standard free-energy change Δ G ° of a reaction therefore determines its chemical equilibrium and predicts in which direction the reaction will proceed under any given set of conditions.

In order for such reactions to proceed, an additional source of energy is required. The conversion of A to B is energetically unfavorable, so the reaction proceeds in the reverse rather than the forward direction.

However, the reaction can be driven in the forward direction by coupling the conversion of A to B with an energetically favorable reaction, such as:. The Δ G of the combined reaction is the sum of the free-energy changes of its individual components, so the coupled reaction is energetically favorable and will proceed as written.

Thus, the energetically unfavorable conversion of A to B is driven by coupling it to a second reaction associated with a large decrease in free energy.

Enzymes are responsible for carrying out such coupled reactions in a coordinated manner. The cell uses this basic mechanism to drive the many energetically unfavorable reactions that must take place in biological systems. The bonds between the phosphates in ATP are known as high-energy bonds because their hydrolysis is accompanied by a relatively large decrease in free energy.

There is nothing special about the chemical bonds themselves; they are called high-energy bonds only because a large amount of free energy is released when they are hydrolyzed within the cell. Actual intracellular concentrations of P i are approximately 10 -2 M, and intracellular concentrations of ATP are higher than those of ADP.

ATP as a store of free energy. The bonds between the phosphate groups of ATP are called high-energy bonds because their hydrolysis results in a large decrease in free energy. ATP can be hydrolyzed either to ADP plus a phosphate group HPO 4 2- or to AMP more Alternatively, ATP can be hydrolyzed to AMP plus pyrophosphate PP i.

This reaction yields about the same amount of free energy as the hydrolysis of ATP to ADP does. However, the pyrophosphate produced by this reaction is then itself rapidly hydrolyzed, with a Δ G similar to that of ATP hydrolysis.

Thus, the total free-energy change resulting from the hydrolysis of ATP to AMP is approximately twice that obtained by the hydrolysis of ATP to ADP. Because of the accompanying decrease in free energy, the hydrolysis of ATP can be used to drive other energy-requiring reactions within the cell.

For example, the first reaction in glycolysis discussed in the next section is the conversion of glucose to glucosephosphate. The reaction can be written as follows:. Other molecules, including other nucleoside triphosphates e. For most reactions, however, ATP provides the free energy.

The energy-yielding reactions within the cell are therefore coupled to ATP synthesis, while the energy-requiring reactions are coupled to ATP hydrolysis.

The high-energy bonds of ATP thus play a central role in cell metabolism by serving as a usable storage form of free energy.

The breakdown of carbohydrates, particularly glucose, is a major source of cellular energy. The complete oxidative breakdown of glucose to CO 2 and H 2 O can be written as follows:. To harness this free energy in usable form, glucose is oxidized within cells in a series of steps coupled to the synthesis of ATP.

Glycolysis , the initial stage in the breakdown of glucose, is common to virtually all cells. Glycolysis occurs in the absence of oxygen and can provide all the metabolic energy of anaerobic organisms.

In aerobic cells, however, glycolysis is only the first stage in glucose degradation. The reactions of glycolysis result in the breakdown of glucose into pyruvate, with the net gain of two molecules of ATP Figure 2.

The initial reactions in the pathway actually consume energy, using ATP to phosphorylate glucose to glucosephosphate and then fructosephosphate to fructose-1,6-bisphosphate. The enzymes that catalyze these two reactions—hexokinase and phosphofructokinase, respectively—are important regulatory points of the glycolytic pathway.

The key control element is phosphofructokinase, which is inhibited by high levels of ATP. Inhibition of phosphofructokinase results in an accumulation of glucosephosphate, which in turn inhibits hexokinase. Thus, when the cell has an adequate supply of metabolic energy available in the form of ATP, the breakdown of glucose is inhibited.

Metabolism pronounced: meh-TAB-uh-liz-um is the chemical reactions in the body's cells that change food into energy. Our bodies need this energy to do everything from moving to thinking to growing. Specific proteins in the body control the chemical reactions of metabolism. Thousands of metabolic reactions happen at the same time — all regulated by the body — to keep our cells healthy and working.

After we eat food, the digestive system uses enzymes to:. The body can use sugar, amino acids, and fatty acids as energy sources when needed. These compounds are absorbed into the blood, which carries them to the cells. After they enter the cells, other enzymes act to speed up or regulate the chemical reactions involved with "metabolizing" these compounds.

During these processes, the energy from these compounds can be released for use by the body or stored in body tissues, especially the liver, muscles, and body fat.

Anabolism pronounced: uh-NAB-uh-liz-um , or constructive metabolism, is all about building and storing. It supports the growth of new cells, the maintenance of body tissues, and the storage of energy for future use. In anabolism, small molecules change into larger, more complex molecules of carbohydrates, protein, and fat.

Catabolism pronounced: kuh-TAB-uh-liz-um , or destructive metabolism, is the process that produces the energy needed for all activity in the cells. Cells break down large molecules mostly carbs and fats to release energy.

This provides fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. As complex chemical units break down into more simple substances, the body releases the waste products through the skin, kidneys, lungs, and intestines.