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What Is The Conversion Of Acetyl Coa Into Ketone Bodies

Gs L36 Liver Metabolism-fasting Fat Oxidation & Ketogenesis

Gs L36 Liver Metabolism-fasting Fat Oxidation & Ketogenesis

Start Quiz! brain, erythrocytes, and adrenal medulla, cannot use fatty acids for energy fatty acids must first be released from triacylglycerols which are stored in adipose tissue, a process called lipolysis whenever the concentration of FA's increases in the blood which occurs normally between meals (fasted state) and also during periods of prolonged fasting or starvation the mitochondria matrix acetyl CoA and NADH/ FADH2 products which enter the TCA cycle and electron transport chain, respectively, thus generating significant amounts of ATP liver is unable to oxidize the ketone bodies it synthesizes, so they are exported into the blood and delivered primarily to the brain ketone bodies can not only supply energy to the brain in periods of long fasting but it can spare muscle protein which would have been degraded for gluconeogenesis Continue reading >>

Lipogenesis From Ketone Bodies In Rat Brain. Evidence For Conversion Of Acetoacetate Into Acetyl-coenzyme A In The Cytosol

Lipogenesis From Ketone Bodies In Rat Brain. Evidence For Conversion Of Acetoacetate Into Acetyl-coenzyme A In The Cytosol

The metabolism of acetoacetate via a proposed cytosolic pathway in brain of 1-week-old rats was investigated. (-)-Hydroxycitrate, an inhibitor of ATP citrate lyase, markedly inhibited the incorporation of carbon from labelled glucose and 3-hydroxybutyrate into cerebral lipids, but had no effect on the incorporation of labelled acetate and acetoacetate into brain lipids. Similarly, n-butylmalonate and benzene-1,2,3-tricarboxylate inhibited the incorporation of labelled 3-hydroxybutyrate but not of acetoacetate into cerebral lipids. These inhibitors had no effect on the oxidation to 14CO2 of the labelled substrates used. (-)-Hydroxycitrate decreased the incorporation of 3H from 3H2O into cerebral lipids by slices metabolizing either glucose or 3-hydroxybutyrate, but not in the presence of acetoacetate. (-)-Hydroxycitrate also differentially inhibited the incorporation of [2-14C]-leucine and [U-14C]leucine into cerebral lipids. The data show that, although the acetyl moiety of acetyl-CoA generated in brain mitochondria is largely translocated as citrate from these organelles to the cytosol, a cytosolic pathway exists by which acetoacetate is converted directly into acetyl-COA in this cellular compartment. Continue reading >>

Ketone Bodies

Ketone Bodies

Ketone bodies Acetone Acetoacetic acid (R)-beta-Hydroxybutyric acid Ketone bodies are three water-soluble molecules (acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone) that are produced by the liver from fatty acids[1] during periods of low food intake (fasting), carbohydrate restrictive diets, starvation, prolonged intense exercise,[2], alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus. These ketone bodies are readily picked up by the extra-hepatic tissues, and converted into acetyl-CoA which then enters the citric acid cycle and is oxidized in the mitochondria for energy.[3] In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids. Ketone bodies are produced by the liver under the circumstances listed above (i.e. fasting, starving, low carbohydrate diets, prolonged exercise and untreated type 1 diabetes mellitus) as a result of intense gluconeogenesis, which is the production of glucose from non-carbohydrate sources (not including fatty acids).[1] They are therefore always released into the blood by the liver together with newly produced glucose, after the liver glycogen stores have been depleted (these glycogen stores are depleted after only 24 hours of fasting)[1]. When two acetyl-CoA molecules lose their -CoAs, (or Co-enzyme A groups) they can form a (covalent) dimer called acetoacetate. Beta-hydroxybutyrate is a reduced form of acetoacetate, in which the ketone group is converted into an alcohol (or hydroxyl) group (see illustration on the right). Both are 4-carbon molecules, that can readily be converted back into acetyl-CoA by most tissues of the body, with the notable exception of the liver. Acetone is the decarboxylated form of acetoacetate which cannot be converted Continue reading >>

Ketone Bodies As Signaling Metabolites

Ketone Bodies As Signaling Metabolites

Outline of ketone body metabolism and regulation. The key irreversible step in ketogenesis is synthesis of 3-hydroxy-3-methylglutaryl-CoA by HMGCS2. Conversely, the rate limiting step in ketolysis is conversion of acetoacetate to acetoacetyl-CoA by OXCT1. HMGCS2 transcription is heavily regulated by FOXA2, mTOR, PPARα, and FGF21. HMGCS2 activity is post-translationally regulated by succinylation and acetylation/SIRT3 deacetylation. Other enzymes are regulated by cofactor availability (e.g., NAD/NADH2 ratio for BDH1). All enzymes involved in ketogenesis are acetylated and contain SIRT3 deacetylation targets, but the functional significance of this is unclear other than for HMGCS2. Although ketone bodies are thought to diffuse across most plasma membranes, the transporter SLC16A6 may be required for liver export, whereas several monocarboxylic acid transporters assist with transport across the blood–brain barrier. Abbreviations: BDH1, β-hydroxybutyrate dehydrogenase; FGF21, fibroblast growth factor 21; FOXA2, forkhead box A2; HMGCS2, 3-hydroxy-3-methylglutaryl (HMG)-CoA synthase 2; HMGCL, HMG-CoA lyase; MCT1/2, monocarboxylic acid transporters 1/2; mTOR, mechanistic target of rapamycin; OXCT1, succinyl-CoA:3-ketoacid coenzyme A transferase; PPARα, peroxisome proliferator-activated receptor α; SIRT3, sirtuin 3; SLC16A6, solute carrier family 16 (monocarboxylic acid transporter), member 6; TCA cycle, tricarboxylic acid cycle. Continue reading >>

Ketogenesis (biosynthesis Of Ketone Bodies)

Ketogenesis (biosynthesis Of Ketone Bodies)

In humans, liver mitochondria have capacity to divert any excess acetyl-CoA formed in the liver during oxidation of fatty acids or oxidation of pyruvate that exceed capacity of citric acid cycle to undergo conversion to the ketone bodies. ketone bodies : [acetoacetate, D-β-hydroxybutyrate& acetone (non metabolizable side product)] for export to other tissues, where they can reconvert to acetyl CoA & oxidized by citric acid cycle. * Ketone bodies are important sources of energy for the peripheral tissues because: They are soluble in aqueous solution (don't need to be incorporated into lipoproteins or carried by albumin like lipid). 2. Produced in liver during periods when acetyl-CoA present exceed the oxidative capacity of the liver. How 3. They are used in proportion to their concentration in the blood by extrahepatic tissues (skeletal & cardiac muscle & renal cortex). Brain, heart & muscle can use ketone bodies to meet their energy needs if the blood levels rise sufficiently (during prolonged periods of fasting). Why ketone bodies synthesized by the liver: The production and export of ketone bodies from the liver to extrahepatic tissues allow continued oxidation of fatty acids in the liver when acetyl-CoA is not being oxidized in the citric acid cycle. * Synthesis of ketone bodies 1-Formation of acetoacetyl CoA can occur by one of 2 processes: a. Incomplete breakdown of fatty acid. b. Enzymatic condensation of two molecules of acetyl-CoA, which catalyzed by thiolase (the reversal of thiolase reaction of fatty acid oxidation). 2- The acetoacetyl-CoA, condenses with 3rd molecule of acetyl-CoA to form β -hydroxy- β -methylglutaryl-CoA (HMG-CoA) catalyzed by HMG-CoA synthase (the rate limiting step in the synthesis of ketone bodies & present in significant quantit Continue reading >>

Selected Solutions To End Of Chapter 17 Problems

Selected Solutions To End Of Chapter 17 Problems

1. Where is the energy in triacylglycerols? The glycerol or fatty acids? Of course, there is so much more fatty acids (long carbon chains) than the three carbon glycerol. But is that all there is, NO! All of glycerol carbons are alcohols, whereas all most all (except for one carbon) all the carbons are alkanes, with a few alkenes tossed in for good measure. Each of these carbons are more reduced than the alcohol carbons in glycerol. 2. Fuel reserves in the average, 70 kg, human. Data: the energy in triacylglycerols is 38 kJ/g and like it or not,15% of the average human is pure fat. The basic energy requirement for the average human is 2,000 dietary calories/day = 8,400 kJ/day. And, 1 lb = 0.454 kg. A dietary calorie is 103 calories. a. What is the total energy reserve in the average human? (7 x 104 g)(0.15)(38 kJ/g) = 4.0 x 105 kJ or in calories = 9.5 x 104 dietary calories. b. How long could this poor average human being survive on fat? (given water,etc.) (4.0 x 105 kJ) / (8,400 kJ/day) = 47.6 days c. What is the weight loss per day under these conditions? = 0.22 kg/day or 0.48 lb/day 3. See how the first three reactions in β-oxidation are similar to CAC reactions: Succinate + FAD Fumarate + FADH2 ane ene Fatty acyl-CoA + FAD trans-Δ2-enoyl CoA + FADH2 Fumarate + H2O Malate ene hydroxy trans-Δ2-enoyl CoA L-β-hydroxyacyl-CoA Malate + NAD+ oxaloacetate + NADH hydroxyl keto L-β-hydroxyacyl-CoA +NAD+ β-ketoacyl-CoA 4. Each cycle of β-oxidation produces an acetyl-CoA. How many β-oxidation cycles does it take to breakdown oleic acid, 18:1 (Δ9)? Answer = 7. (Hint: the last reaction produces 2 acetyl-CoAs) 9. Compartmentalization of β-oxidation (it occurs in the mitochondria). Palmitic acid taken up by a cell gets converted to palmitoyl-CoA in Continue reading >>

Metabolism

Metabolism

Reactions and Metabolic Pathways A progression of metabolic reactions from beginning to end is called a pathway Intermediates of reactions Anabolic pathways Catabolic pathways Energy for the cell Energy used in cells come from the chemical bonds found between atoms in carbohydrate, fat, protein, and alcohol Most energy is from the sun and involved in reactions converting carbon dioxide and water into glucose – (photosynthesis) Glucose used in cell respiration to produce ATP used by all reactions in all cells Types of energy: chemical, mechanical, electrical, osmotic Oxidation-Reduction Reactions A substance is oxidized when it loses one or more electrons A substance is reduced when it gains one or more electrons Oxidation-reduction reactions are controlled by enzymes Antioxidants – compounds that donate electrons to oxidized compounds, putting them into a more reduced (stable) state Oxidized compounds tend to be highly reactive Vitamins E and C are antioxidants Remember phytochemicals! Glycolysis, Citric Acid Cycle (also called Krebs Cycle), and Electron Transport Chain (ETC) Glycolysis Occurs in the cytosol of the cell Begin process with glucose 2 ATP used 4 ATP produced = 2 ATP net Water molecule is removed Hydrogen atoms removed from intermediates by NAD molecules 2 pyruvate molecules produced at end of the pathway If no oxygen present in the cell then pyruvates are converted into lactate – this process is called anaerobic respiration Intermediate step: Pyruvate to Acetyl CoA (occurs in the mitochodria) Citric Acid Cycle Occurs in the mitochondria Acetyl CoA added to compound in the cycle Hydrogens are removed by NAD molecules and FAD molecules Carbon dioxide is removed from intermediates GTP produced (a usable energy source like ATP) Electron Transport Chain H Continue reading >>

6.9: Ketone Body Synthesis

6.9: Ketone Body Synthesis

In ketone body synthesis, an acetyl-CoA is split off from HMG-CoA, yielding acetoacetate, a four carbon ketone body that is somewhat unstable, chemically. It will decarboxylate spontaneously to some extent to yield acetone. Ketone bodies are made when the blood levels of glucose fall very low. Ketone bodies can be converted to acetyl-CoA, which can be used for ATP synthesis via the citric acid cycle. People who are very hypoglycemic (including some diabetics) will produce ketone bodies and these are often first detected by the smell of acetone on their breath. Figure 6.9.1: Ketone Body Reactions Acetone is of virtually no use for energy production since it is not readily converted to acetyl-CoA. Consequently, cells convert acetoacetate into beta- hydroxybutyrate, which is more chemically stable. Though technically not a ketone, beta-hydroxybutyrate is frequently referred to as a ketone body. Upon arrival at a target cell, it can be oxidized back to acetoacetate with conversion to acetyl-CoA. Both acetoacetate and beta-hydroxybutyrate can cross the blood-brain barrier and provide important energy for the brain when glucose is limiting. Continue reading >>

Chapter 25: Lipids: Lipolysis, Fatty Acid Oxidation, And Ketogenesis

Chapter 25: Lipids: Lipolysis, Fatty Acid Oxidation, And Ketogenesis

Chapter 25: Lipids: Lipolysis, Fatty Acid Oxidation, and Ketogenesis Parents of a 3-month-old infant arrive at the ER agitated and frightened by the extreme lethargy and near comatose state of their child. Examination shows the infant to be severely hypoglycemic accompanied by low measurable ketones in the urine and blood. Blood analysis also indicates an elevation in butyric and propionic acids and as well as C8-acylcarnitines. A deficiency in which of the following enzymes is most likely responsible for these observations? B. hormone-sensitive lipase (HSL) C. lipoprotein lipase (LPL) D. long-chain acyl-CoA dehydrogenase (LCAD) E. medium-chain acyl-CoA dehydrogenase (MCAD) Answer E: In infants, the supply of glycogen lasts less than 6 hours and gluconeogenesis is not sufficient to maintain adequate blood glucose levels. Normally, during periods of fasting (in particular during the night) the oxidation of fatty acids provides the necessary ATP to fuel hepatic gluconeogenesis as well as ketone bodies for nonhepatic tissue energy production. In patients with MCAD deficiency there is a drastically reduced capacity to oxidize fatty acids. This leads to an increase in glucose usage with concomitant hypoglycemia. The deficit in the energy production from fatty acid oxidation, necessary for the liver to use other carbon sources, such as glycerol and amino acids, for gluconeogenesis further exacerbates the hypoglycemia. Normally, hypoglycemia is accompanied by an increase in ketone formation from the increased oxidation of fatty acids. In MCAD deficiency there is a reduced level of fatty acid oxidation, hence near-normal levels of ketones are detected in the serum. Oxidation of fatty acids requires the input of energy in the form of ATP. Which of the following enzyme activities Continue reading >>

Ketone Bodies Liver Mitochondria Have The Capacity To Convert Acetyl Coa Derived From Fatty Acid Oxidation Into Ketone Bodies Which Are: 1- Acetoacetic.

Ketone Bodies Liver Mitochondria Have The Capacity To Convert Acetyl Coa Derived From Fatty Acid Oxidation Into Ketone Bodies Which Are: 1- Acetoacetic.

Presentation on theme: "Ketone bodies Liver mitochondria have the capacity to convert acetyl CoA derived from fatty acid oxidation into ketone bodies which are: 1- Acetoacetic."— Presentation transcript: 1 Ketone bodies Liver mitochondria have the capacity to convert acetyl CoA derived from fatty acid oxidation into ketone bodies which are: 1- Acetoacetic acid 2- β-hydroxy butyric acid 3- Acetone Functions of ketone bodies: 1-Used as source of energy. They are reconverted into acetyl CoA which is oxidized in Kreb's cycle to give energy. 2- In prolonged fasting and starvation, ketone bodies can be used as source of energy by most tissues except liver. N.B. In fasting, most tissues get energy from oxidation of both ketone bodies and fatty acids, but the brain gets its energy from oxidation of ketone bodies. Brain never oxidizes fatty acids. 2 Synthesis of ketone bodies by the liver (Ketogenesis) Site of ketogenesis: Mitochondria of liver cells due to high activity of HMG-CoA synthase, HMG- CoA- lyase. Steps of ketogenesis: See Figure (not required) 1- 3 molecules of acetyl CoA are condensed to give 3-hydroxy 3-glutaryl CoA (HMG CoA). This step is catalyzed by HMG CoA synthase (the key enzyme) 2- HMG CoA is then broken by HMG CoA lyase enzyme to acetoacetate. 3- Part of acetoacetate is converted into acetone and part is converted into β-hydroxy butyric acid Notes on ketogenesis: 1- HMG- CoA synthase is the rate limiting enzyme in the synthesis of ketone bodies and is present in significant amounts only in the liver. 3- Acetone is a volatile, nonmetabolized product that can be released in the breath. 3 Regulation of ketogenesis: Regulation of HMG-CoA synthase A- Inhibited after CHO diet (after meal): CHO diet inhibits HMG-CoA synthase. In addition, after meal, insulin i Continue reading >>

Ketone Bodies Metabolism

Ketone Bodies Metabolism

1. Metabolism of ketone bodies Gandham.Rajeev Email:[email protected] 2. • Carbohydrates are essential for the metabolism of fat or FAT is burned under the fire of carbohydrates. • Acetyl CoA formed from fatty acids can enter & get oxidized in TCA cycle only when carbohydrates are available. • During starvation & diabetes mellitus, acetyl CoA takes the alternate route of formation of ketone bodies. 3. • Acetone, acetoacetate & β-hydroxybutyrate (or 3-hydroxybutyrate) are known as ketone bodies • β-hydroxybutyrate does not possess a keto (C=O) group. • Acetone & acetoacetate are true ketone bodies. • Ketone bodies are water-soluble & energy yielding. • Acetone, it cannot be metabolized 4. CH3 – C – CH3 O Acetone CH3 – C – CH2 – COO- O Acetoacetate CH3 – CH – CH2 – COO- OH I β-Hydroxybutyrate 5. • Acetoacetate is the primary ketone body. • β-hydroxybutyrate & acetone are secondary ketone bodies. • Site: • Synthesized exclusively by the liver mitochondria. • The enzymes are located in mitochondrial matrix. • Precursor: • Acetyl CoA, formed by oxidation of fatty acids, pyruvate or some amino acids 6. • Ketone body biosynthesis occurs in 5 steps as follows. 1. Condensation: • Two molecules of acetyl CoA are condensed to form acetoacetyl CoA. • This reaction is catalyzed by thiolase, an enzyme involved in the final step of β- oxidation. 7. • Acetoacetate synthesis is appropriately regarded as the reversal of thiolase reaction of fatty acid oxidation. 2. Production of HMG CoA: • Acetoacetyl CoA combines with another molecule of acetyl CoA to produce β-hydroxy β-methyl glutaryl CoA (HMC CoA). • This reaction is catalyzed by the enzyme HMG CoA synthase. 8. • Mitochondrial HMG CoA is used for ketogenesis. Continue reading >>

Biochemistry 12: Diabetes

Biochemistry 12: Diabetes

These are notes from lecture 12 of Harvard Extension’s biochemistry class. starvation The first priority is to provide enough glucose to tissues that are solely dependent on glucose – the brain and red blood cells. It was long thought that fatty acids cannot be converted to glucose, though there is now some evidence that this conversion may occur under some circumstances. Amino acids are a poor fuel source because they’re not stored (no equivalent of glycogen or triacylglycerol), so you’d just be catabolizing proteins you need to live. Starvation occurs in stages. Exogenous glucose can be used for the first 4 hours after a meal. Then glycogen reserves kick in from hour 4 to hour ~28. As the glycogen mobilization peaks around hour 8, gluconeogenesis begins, and can continue full steam for about 2 days, after which it dampens slightly but can continue for up to 40 days at a lower level. During days 2-24, the kidney begins gluconeogenesis and the brain begins using ketone bodies. In Stage V (days 24-40), the liver and kidney continue to do gluconeogenesis and the brain relies solely on ketone bodies. Muscle protein degradation is about 75 g/day at day 3 of starvation, 20 g/day at day 40 of starvation. The initial sources of proteins are rapid turnover proteins from the intestinal epithelium and secreted pancreatic proteins. After three days, the liver forms ketone bodies (from fatty acid catabolism) which become the predominant energy source, preventing additional protein degradation. After an average of 40 days (more if you have more adipose tissue), TAG stores are depleted, and protein degradation increases again, impacting heart, liver and kidney function and leading ultimately to death. See [Berg 2002] for an overview of all this, esp. muscle protein degradatio Continue reading >>

Biochemistry Ii (bio 3362), Spring, 1998

Biochemistry Ii (bio 3362), Spring, 1998

FIGURES 7.1 Overview of conversion of propionyl-CoA to succinate. 7.2 Review of biotin in carboxylation reactions. I. b -oxidation of odd-carbon fatty acids A. Odd-carbon fatty acids, which yield propionyl-CoA upon b-oxidation, are common in many mammalian (including human) diets. A series of three enzymatic reactions convert propionyl-CoA to succinate in the mitochondria. 1. Besides b -oxidation of odd-carbon fatty acids, there are other sources of propionyl-CoA that are also metabolized to succinate. a. In ruminants, bacterial fermentation of plant material produces a lot of propionic acid, which is converted to propionyl-CoA, and then to succinate. b. In non-ruminant animals, propionyl-CoA is produced as a product of catabolism of valine, isoleucine, methionine, and threonine. It is also produced by degradation of the side chain of cholesterol. B. Propionyl-CoA carboxylase. 1. Addition of carboxylate group is stereospecific to produce (S)-methylmalonyl-CoA (the same as D-methylmalonyl-CoA). 2. There is an inborn error of metabolism that results from a deficiency in propionyl-CoA carboxylase. Patients with this disease have elevated levels of propionate in their blood, along with a variety of other symptoms. In its severest form the disease is lethal. 7.3 Epimerase mechanism 7.4 Review of active B-12 formation. 7.5 Mechanism of the mutase 7.6 TCA cycle 7.7 Export of malate from mitochondria. 7.8 Malic enzyme. C. Methylmalonyl-CoA epimerase. 1. This reaction, like many other CoA derivatives, involves the (relatively) acidic proton at the a-carbon, with resonance stabilization of the carbanion intermediate. D. Methylmalonyl-CoA mutase. 1. This is an intramolecular rearrangement catalyzed by a vitamin B-12-dependent reaction to produce succinyl-CoA. 2. There is in inborn Continue reading >>

Mbm 16 €“ Ketone Body Metabolism. Purpose, Connections And Control

Mbm 16 €“ Ketone Body Metabolism. Purpose, Connections And Control

MedSoc Teaching MBM Session 5 Habillan Naathan (mzyhn2) Objectives * Understand the role of ketone bodies in human metabolism. * Be able to describe the ketone bodies their metabolism. * Have an overview of the role of ketone bodies in diabetes and starvation. Ketone Bodies ï€ Starvation: ï€ blood glucose drops very low, endangering the brain ï€ Mobilisation of fatty acids from adipose tissue (glucagon high) BUT- PROBLEM! ï€ Brain cannot use ….. ï€ Liver: TCA cycle cannot utilise all the …. from β-oxidation ï‚· citrate synthase not active enough ï‚® accumulation of acetyl CoA ï€ Liver: acetylCoA diverted to ketone bodies ï€ Can be utilised by muscle, kidney and eventually the brain under starvation conditions or in diabetes ï€ When in excess, acetyl CoA produced from β-oxidation of fatty acids, is converted into …………………….. and ………………………. ï€ Together with acetone these compounds collectively termed ketone bodies ï€ Acetone formed during ketosis but cannot be utilized ï‚® excreted on breath producing typical smell of a ketotic individual (acetone not metabolized) ï€ Ketosis occurs during starvation and diabetes (when glucose utilisation is impaired) MedSoc Teaching MBM Session 5 Habillan Naathan (mzyhn2) ï€ Babies can become ketotic quickly due to small glycogen stores Ketone Body Synthesis ï€ 2 molecules acetyl CoA initially condense to form acetoacetyl CoA ï‚® reverse of thiolysis step in β-oxidation ï€ Acetoacetyl CoA reacts with another molecule of acetyl CoA to form ………………………………………. (HMG CoA) ï€ Th Continue reading >>

Acetyl-coa

Acetyl-coa

Definition: Acetyl-CoA is an important molecule in metabolism, used in many biochemical reactions. Its main use is to convey the carbon atoms within the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production. Its is the base of the biosynthesis of fatty acids and cholesterol. Acetyl-CoA is also an important component in the biogenic synthesis of the neurotransmitter acetylcholine. Choline, in combination with Acetyl-CoA, is catalyzed by the enzyme choline acetyltransferase to produce acetylcholine and a coenzyme a byproduct. Structure In chemical structure, acetyl-CoA is the thioester between coenzyme A (a thiol) and acetic acid (an acyl group carrier). Acetyl-CoA is produced during the second step of aerobic cellular respiration, pyruvate decarboxylation, which occurs in the matrix of the mitochondria. Acetyl-CoA then enters the citric acid cycle (Krebs cycle). Metabolism Acetyl-CoA is produced in mitochondria through the metabolism of fatty acids and the oxidation of pyruvate to acetyl-CoA. When ATP is needed, this acetyl-CoA can enter the Krebs cycle to drive oxidative phosphorylation. When ATP supplies are abundant, the acetyl-CoA can be diverted to other purposes like energy storage in the form of fatty acids. The biosynthesis of fatty acids from this acetyl-CoA cannot take place directly however, since it is produced inside mitochondria while fatty acid biosynthesis occurs in the cytosol. There is not a mechanism that directly transports acetyl-CoA out of mitochondria. To be transported, the acetyl-CoA must be chemically converted to citric acid using a pathway called the tricarboxylate transport system. Inside mitochondria, the enzyme citrate synthase joins acetyl-CoA with oxaloacetate to make citrate. This citrate is transported Continue reading >>

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