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What Is The Conversion Of Acetyl Coa Into Ketone Bodies

Ketone Body Metabolism

Ketone Body Metabolism

Ketone body metabolism includes ketone body synthesis (ketogenesis) and breakdown (ketolysis). When the body goes from the fed to the fasted state the liver switches from an organ of carbohydrate utilization and fatty acid synthesis to one of fatty acid oxidation and ketone body production. This metabolic switch is amplified in uncontrolled diabetes. In these states the fat-derived energy (ketone bodies) generated in the liver enter the blood stream and are used by other organs, such as the brain, heart, kidney cortex and skeletal muscle. Ketone bodies are particularly important for the brain which has no other substantial non-glucose-derived energy source. The two main ketone bodies are acetoacetate (AcAc) and 3-hydroxybutyrate (3HB) also referred to as β-hydroxybutyrate, with acetone the third, and least abundant. Ketone bodies are always present in the blood and their levels increase during fasting and prolonged exercise. After an over-night fast, ketone bodies supply 2–6% of the body's energy requirements, while they supply 30–40% of the energy needs after a 3-day fast. When they build up in the blood they spill over into the urine. The presence of elevated ketone bodies in the blood is termed ketosis and the presence of ketone bodies in the urine is called ketonuria. The body can also rid itself of acetone through the lungs which gives the breath a fruity odour. Diabetes is the most common pathological cause of elevated blood ketones. In diabetic ketoacidosis, high levels of ketone bodies are produced in response to low insulin levels and high levels of counter-regulatory hormones. Ketone bodies The term ‘ketone bodies’ refers to three molecules, acetoacetate (AcAc), 3-hydroxybutyrate (3HB) and acetone (Figure 1). 3HB is formed from the reduction of AcAc i Continue reading >>

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 >>

Multiple Choice Quiz 1

Multiple Choice Quiz 1

(See related pages) 1 Which one of the following would not be a nutrient? 2 Most vitamins, minerals, and water all have this in common: 3 When the body metabolizes nutrients for energy, fats yield about _______ times the energy as carbohydrates or proteins. 4 A calorie is the amount of energy necessary to raise the temperature of one gram of _________ one degree __________. 5 One piece of apple pie would yield about 6 The disaccharide that most people think of as table sugar is 7 When lactose is digested, it yields two monosaccharides called 8 The complex carbohydrate (polysaccharide) that is digested to the monosaccharide, glucose, and is found in vegetables, fruits, and grains and is called 9 If excess glucose is present in the body, the glucose first will be stored as __________ in muscle and the liver. 10 Triglycerides that contain one or more double covalent bonds between carbon atoms of their fatty acids are called 11 Bubbling hydrogen gas through polyunsaturated vegetable oil will cause the oil to become more 12 The lipid that is a component of the plasma membrane and can be used to form bile salts and steroid hormones is 13 The American Heart Association recommends that saturated fats should contribute no more than 10% of total fat intake. Excess fats, especially cholesterol and saturated fat, can increase the risk of 16 The daily-recommended consumption amount of protein for a healthy adult is about _____% of total kilocalorie intake per day. 20 Inorganic nutrients that are necessary for normal metabolism are called 23 When a molecule loses an electron, that molecule is said to be ___________ and often a(n) _____________ ion is lost along with the electron. 25 When a hydrogen ion and an associated electron are lost from a nutrient molecule, which of the followi 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 >>

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 >>

Regulation Of Ketone Body And Coenzyme A

Regulation Of Ketone Body And Coenzyme A

METABOLISM IN LIVER by SHUANG DENG Submitted in partial fulfillment of the requirements For the Degree of Doctor of Philosophy Dissertation Adviser: Henri Brunengraber, M.D., Ph.D. Department of Nutrition CASE WESTERN RESERVE UNIVERSITY August, 2011 SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of __________________ ____________ _ _ candidate for the ________________________________degree *. (signed) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. Shuang Deng (chair of the committee) Edith Lerner, PhD Colleen Croniger, PhD Henri Brunengraber, MD, PhD Doctor of Philosophy Janos Kerner, PhD Michelle Puchowicz, PhD Paul Ernsberger, PhD I dedicate this work to my parents, my son and my husband iv TABLE OF CONTENTS Table of Contents…………………………………………………………………. iv List of Tables………………………………………………………………………. viii List of Figures……………………………………………………………………… ix Acknowledgements………………â 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 >>

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 >>

Acetyl Coa - Cross Roads Compound

Acetyl Coa - Cross Roads Compound

Metabolic Fates of Acetyl CoA: If you reflect on both the content lipid metabolism and the previous carbohydrate metabolism, you can appreciate that there is a special central role for acetyl CoA. Acetyl CoA acts both as a metabolic "receiving and shipping department" for all classes of biomolecules and as a major source of useful metabolic energy. The diagram on the left summarizes all metabolism and the central role of acetyl CoA. The diagram the next lower panel focuses on other functions as well. The interactions of amino acids with acetyl CoA and the citric acid cycle will be studied in protein metabolism. Notice that acetyl CoA can react "reversibly" in the degradation or synthesis of lipids and amino acids. This is not the case with carbohydrate metabolism. In mammals, it is impossible to use acetyl CoA to make carbohydrates. Synthesis of Cholesterol and other Steroids: Without going into detail, acetyl CoA forms the basis from which the fairly complicated steroids are synthesized. Some steroids of importance include cholesterol, bile salts, sex hormones, aldosterone, and cortisol. The major concern about cholesterol in the diet is muted somewhat by the knowledge that the liver can and does synthesize all of the cholesterol that the body needs. Excess cholesterol, whether from food or synthesized by the liver, ends up in the blood stream where it builds up on the artery walls. It has been determined that cholesterol levels can be controlled by lowering the amount of saturated fat and increasing the unsaturated fats. Unsaturated fats seem to speed the rate at which cholesterol breaks down in the blood. Controlling fats and cholesterol in the diet can significantly affect the levels of these substances in the blood. Lipogenesis: Since carbohydrates are the major pa Continue reading >>

Chapter 7

Chapter 7

Metabolic pathway Catabolism Anabolism Mitochondria ATP NADH FADH GTP ADP AMP NADPH A series of chemical reactions that either break down a large compound into small pieces or synthesize bigger compounds from smaller molecules Breaking down large particles into smaller ones. Process which cells change smaller compounds into larger more complex ones. Where most of the ATP is captured when being made from CHO,PRO or FAT. Called the "power plant" of the cells. High energy molecules which is what fuels most of the cells and is used to synthesize molecules. Reduced form of NAD, acts as an electron carrier in cells and undergoes oxidation and reduction Reduced form of FAD, also acts like an electron carrier and undergoes oxidation and reduction Similar to ATP, but with 3 phosphates linked to guanosine. Compound produced upon hydrolysis of ATP and is used to synthesize ATP Product of hydrolysis from ADP and nucleic acids. Reduced form of NADP. Also acts as an electron carrier in cells and undergoes reduction and oxidation. Glycolysis Aerobic Anaerobic Pyruvate Lactate Krebs cycle Citrate Oxalate Anaerobic pathway of breaking down glucose molecules into 2 molecules of pyruvate and creates 2 molecules of ATP and NADH. Occurs in cytosol. Needs oxygen in order for metabolic pathway to happen No need of oxygen for the metabolic pathway to happen 3 carbon compound that is created from the breakdown of glucose, can also be derived from amino acids and glycerol. Ionized form of lactic acid and is produced when there is a lack of oxygen in cells to produce pyruvate Also known as citric acid cycle, takes place in mitochondria where acetyl part of acetyl CoA is oxidized to yield 2 CO2, and NADH, FADH2, and GTP. Organic acid which can be found in some leafy green veggies that binds to cal 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 >>

Introduction To Degradation Of Lipids And Ketone Bodies Metabolism

Introduction To Degradation Of Lipids And Ketone Bodies Metabolism

Content: 1. Introduction to degradation of lipids and ketone bodies metabolism 2. Lipids as source of energy – degradation of TAG in cells, β-oxidation of fatty acids 3. Synthesis and utilisation of ketone bodies _ Triacylglycerol (TAG) contain huge amounts of chemical energy. It is very profitable to store energy in TAG because 1 g of water-free TAG stores 5 times more energy than 1 g of hydrated glycogen. Complete oxidation of 1 g of TAG yields 38 kJ, 1g of saccharides or proteins only 17 kJ. Man that weighs 70 kg has 400 000 kJ in his TAG (that weight approximately 10,5 kg). This reserve of energy makes us able to survive starving in weeks. TAG accumulate predominantly in adipocyte cytoplasm. There are more types of fatty acid oxidation. Individual types can be distinguished by different Greek letters. Greek letter denote atom in the fatty acid chain where reactions take place. β-oxidation is of major importance, it is localised in mitochondrial matrix. ω- and α- oxidation are localised in endoplasmic reticulum. Animal cells cannot convert fatty acids to glucose. Gluconeogenesis requires besides other things (1) energy, (2) carbon residues. Fatty acids are rich source of energy but they are not source of carbon residues (there is however one important exception, i.e. odd-numbered fatty acids). This is because cells are not able to convert AcCoA to neither pyruvate, nor OAA. Both carbons are split away as CO2. PDH is irreversible. Plant cells are capable of conversion of AcCoA to OAA in glyoxylate cycle. _ Lipids as source of energy – degradation of TAG in cells, β-oxidation of fatty acids Lipids are used for energy production, this process take place in 3 phases: 1) Lipid mobilisation – hydrolysis of TAG to FA and glycerol. FA and glycerol are transported Continue reading >>

Question: 16- When The Body Is Deficient In Oxaloacetate A) Acetyl Coa From The B-oxdiation Pathway Cannot ...

Question: 16- When The Body Is Deficient In Oxaloacetate A) Acetyl Coa From The B-oxdiation Pathway Cannot ...

16- When the body is deficient in oxaloacetate a) acetyl CoA from the b-oxdiation pathway cannot enter the citric acid cycle b) oxaloacetate is diverted to gluconeogenesis c) acetyl CoA is diverted to form the ketone bodies d) all of the above are true e) none of the above 17- The synthesis of ketone bodies involves a) synthesis of acetoacetyl-CoA by reversal of the thiolase reaction of fatty oxidation b) synthesis of b-hydroxy-b-methylglutaryl-CoA (HMG-CoA) c) cleavage of HMG-CoA to acetoacetate. d) b-Hydroxybutyrate is produced by reduction of acetoacetate. e) all of the above 18- Which of the statements about ketone body production is FALSE? a) Ketone bodies are produced when there is more acetyl-CoA in the liver than can be oxidized in the citric acid cycle. b) Ketone bodies production is not a normal process, and occurs only in diabetes or starvation c) The ketone bodies produced in the body are the free acids and not the CoA esters. d) When fatty acid oxidation in the liver is uncontrolled, ketone body production becomes excessive and life-threatening because these acidic compounds lower the pH of blood e) When fatty acid oxidation 19- In which of the following ways can the 4-carbon compound acetoacetyl CoA produced in fatty acid degradation be further metabolized? a) It can break down further to form acetyl CoA, b) It can be converted to the ketone bodies c) It can be used for synthesis of cholesterol and its many derivatives. d) It can do all of the above e) It can do none of the above 20- Acetyl CoA from the beta-oxidation pathway cannot enter the citric acid cycle in which of these circumstances? a) periods of fasting b) periods of starvation c) diabetes d) when the body is deficient in oxaloacetate e) all of the above 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 >>

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