Class Note for BIOC 460 at UA 3
Class Note for BIOC 460 at UA 3
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Date Created: 02/06/15
Bioc 460 Dr Miesfeld Fall 2008 Lecture 34 Fatty acid oxidation Figure 1 Key Concepts 39539quot p 391 1 Overview of lipid metabolism 39 Reactions of fatty acid oxidation 1 Energy yield from fatty acid oxidation Formation of ketone bodies Tria39cryl lylcemlssmam adipose tissue and released in response to hormones Overview of lipid metabolism G U on Carbohydrate metabolism IS but one D39e a39v r39acylg39Wem EMSwine Triacylglycerols synthesized in the liver from carbohydrates and exported component of energy production and storage In fact a much larger percentage Fatty acids Chylomicrons I VLDL particles of the total energy reserves In animals IS lipids in the form of fat deposits consisting Album39n of energyrich fatty acids As shown in figure 1 there are three basic sources of fatty acids in animals that can be used for energy conversion processes 1 fatty acids present in triacylglycerols figure 2 obtained from the diet 2 fatty acids stored as triacylglycerols in adipose tissue that are released by hydrolysis following Arterlole Capillaries hormone stimulation glucagon or epinephrine signaling and 3 fatty acids synthesized in the liver from excess carbohydrates and exported as triacylglycerols Fatty acids in dietary triacylglycerols are transported from the intestines to the rest ofthe body by large lipoprotein particles called chylomicrons Hormone signaling releases fatty acids from adipose tissue that bind to an abundant transport protein in serum called albumin Lastly fatty acids synthesized in the liver are carried through the body as triacylglycerols by very low density lipoprotein VLDL particles Palmitate is a 016 saturated fatty acid that can be Figure 2 carried through the body as a protein Glycerol fatty acrd complex 0 Fatty acid 2 Fat is stored in fat cells Fatty acid 1 O erO C mm CH3 adipocytes Obesity especially H C77 CH 72 jCli CH ibioiCH childhood obesity can be due to both 3 2 2 F l Venule more fat storage per cell and to a CHZ O mHZ m CH3 larger number of adipocytes figure 2 0 Fatty acid 3 In contrast in normal healthy adults the onset of old age and reduced metabolic rates leads to weight gain resulting primarily from storing more fat per cell although adults can also add more fat cells if they become obese Fat droplet cytoplasm 39 nucleus 1 of 9 pages Bioc 460 Dr Miesfeld Fall 2008 Pathway Questions for Fatty Acid Metabolism 1 What purpose does fatty acid metabolism serve in animals Fatty acid oxidation in mitochondria is responsible for providing energy to cells when glucose levels are low Triacylglycerols stored in adipose tissue of most humans can supply energy to the body for 3 months during starvation Fatty acid synthesis reactions in the cytosol of liver and adipose cells convert excess acetyl CoA that builds up in the mitochondrial matrix when glucose levels are high into fatty acids that can be stored or exported as triacylglycerols Lipid Metabolism 2 What are the net reactions of fatty acid degradation Triglycerides and synthesis for the C18 fatty acid palmitate I 3235 Steroids Fatty acid oxidation Fatty ll Palmitate 7 NAD 7 FAD 8 COA 7 H20 ATP gt adds Cholesterol 8 acetyl CoA 7 NADH 7 FADH2 AMP 2 Pi 7 H Amigo l J Aci s i l a Fatty acid synthesis l 8 Acetyl COA 7 ATP 14 NADPH 14 H gt palmitate 8 COA 7 ADP 7 Pi 14 NADP 6 H20 Citrate Cycle 3 What are the key enzymes in fatty acid 1 metabolism quot Fatty acyl CoA synthetase enzyme catalyzing the quot39 39 quotprimingquot reaction in fatty acid metabolism which converts V f 5 free fatty acids in the cytosol into fatty acylCoA using the energy available from ATP and PPi hydrolysis When 39 quot the energy charge in the cell is low the fatty acylCoA is used for fatty acid oxidation inside the mitochondria however when the energy charge is high the fatty acylCoA is used to synthesize triacylglycerols or membrane lipids Carnitine acyltransferase l catalyzes the commitment step in fatty acid oxidation which links fatty acylCoA molecules to the hydroxyl group of carnitine The activity of carnitine acyltransferase l is inhibited by malonyl CoA the product of the acetylCoA carboxylase reaction which signals that glucose levels are high and fatty acid synthesis is favored Acetyl CoA carboxylase catalyzes the commitment step in fatty acid synthesis using a biotin mediated reaction mechanism that carboxylates acetyl CoA to form the C3 compound malonyl CoA The activity of acetyl CoA carboxylase is regulated by both reversible phosphorylation the active conformation is dephosphorylated and allosteric mechanisms citrate binding stimulates activity palmitoylCoA inhibits activity Fatty acid synthase this large multifunctional enzyme is responsible for catalyzing a series of reactions that sequentially adds C2 units to a growing fatty acid chain covalently attached to the enzyme complex The mechanism involves the linking malonylCoA to an acyl carrier protein followed by a decarboxylation and condensation reaction that extends the hydrocarbon chain 4 What are examples of fatty acid metabolism in real life A variety of foods are prominently advertised as quotnonfatquot even though they can contain a high calorie count coming from 1 carbohydrates Eating too much of these high calorie nonfat foods eg nonfat bagels activates the fatty acid synthesis pathway I resulting in the conversion of acetyl CoA to fatty acids which are es Olestra Bioc 460 Dr Miesfeld Fall 2008 stored as triacylglycerols Olestra is a fat substitute composed of a sucrose molecule with several fatty acids attached Transport and storage of fatty acids and triacylglycerols Much of the triacylglycerol stored in adipose tissue originates from dietary lipids Fats that enter the small intestine from the stomach are insoluble and must be emulsified by bile acids such as glycocholate which are secreted by the bile duct and function as detergents to promote the formation of micelles Lipases are water soluble enzymes in the small intestine that hydrolyze the acyl ester bonds in triacylglycerols to liberate free fatty acids which then pass through the membrane on the lumenal side of intestinal epithelial cells gure 3 Pancreatic lipase cleaves the ester bond at the C1 and C3 carbons to release two free fatty acids and monoacylglyclerol whereas other intestinal lipases cleave at the C2 carbon to generate glycerol and fatty acid The absorption and transport of dietary triacylglycerols can be broken down into ve steps 1 emulsi cation of triacylglycerols by bile acids 2 hydrolysis of fatty acids by intestinal lipases 3 resynthesis of triacylglycerols inside intestinal epithelial cells 4 packaging of triacylglycerols into large lipoprotein particles called chylomicrons and 5 export of the chylomicrons to the lymphatic system Chylomicrons transport the triacylglycerols to adipose tissue for storage and to muscle cells for energy conversion processes Apolipoprotein Cll on the surface of chylomicrons binds to and activates lipoprotein lipase on endothelial cells which leads to the release of fatty acids and glycerol gure 4 Fatty acids diffuse into the endothelial cells and then enter nearby adipose and muscle cells where they are stored or used for energy conversion pathways The glycerol produced by lipoprotein lipase returns to the liver where it is converted to dihydroxyacetone phosphate Two other important apolipoproteins on chylomicrons are apolipoprotein Clll Figure 3 Dietary triacylglycerols emulsified by bile acids r Luminal Side side Bile I ii acid 391 cVquot r g Intestinal g epithelialcell 2 Lipasecleavage V I Fattyaads g resynthesized into a W triacylglycerols Basolateral Triacylglycerols C packaged into Glycerol chylomicrons st 1quot v 9393 Q 2 Fattyacids l Lipase cleavage 7 J Phospholipids a g Intestinal lumen 7 e l 239 Lipoproteins f Figure 4 Chylomicron 39 ApoClll Ape B48 quot Glycerol To I O gt liver 9 2 i 7 Fatty Bleed APO C39 739 39 I Lipoprotein lipase Activated lipoprotein lipase l I 7 Ly 3 Endothelial C l 39 Cell x 7 lg 7 Fatty acids Transporter enter nearby through cells microcapill to distantc 3 of 9 pages Formation of albuminfatty acid complexes Albumin apoC lll and apolipoprotein B48 apoB48 Bloc 460 Dr Miesfeld Fall 2008 Dietary lipids are not the only source oftriacylglycerols stored in adipocytes The liver synthesizes triacylglycerols from fatty acids when glucose levels are high and the amount of acetyl CoA produced exceeds the energy requirements of the cell As shown in gure 5 glucose provides the necessary substrates for triacylglycerol synthesis acetyl 00A for fatty acid synthesis and glycerol using reactions in the gycoytic pathway and the citrate cycle In this metabolic scheme glucose is converted to fructose 16bisphosphate which is cleaved by aldolase to generate dihydroxyacetone phosphate DHAP and glyceraldehyde3 phosphate GAP The DHAP is used to make glycerol3 phosphate and the GAP is converted to pyruvate which is then oxidatively decarboxylated by the mitochondrial enzyme pyruvate dehyd rogenase to form acetyl CoA Citrate synthase the rst enzyme in the citrate cycle combines oxaloacetate and acetyl CoA to generate citrate which is l Carbohydrateg e Glucose gt To quot39 9 adipose 39 39 amp tissue VLDL particle 3 m Glucose Lipoproteins fl l Triacylglycerol A Fatty Acids 3 Fructose16bisphosphate Adoase e9 DHAP 6 Glycem39ap c Q Gchemap A Glyceraldehyde3P dwydmggmm Fatty Fatty Acyl CoA Acid ranyazm P yruvate SyntheSIs WWW l MalonyliCoA Py ruvate Mame Amy0A CoA Pyruvate Malate CO carboxylase C02 dehydrogenase X 2 v 0AA Acet lCoA AcetylCoA 0AA 5mm y 7 lyase CoA f Ova Ely761 J a Citrate trate 39 0 Citrate Cycle 3 Citrate Shuttle High energy charge inhibits citrate cycle Mitochondrion shuttled to the cytosol where it is cleaved by the enzyme citrate lyase to generate acetyl CoA and oxaloacetate This process of shipping acetyl CoA out ofthe mitochondria using citrate and oxaloacetate is called the citrate shuttle and is described later The cytosolic acetyl CoA is converted to malonyl CoA by the enzyme acetyl CoA carboxylase which then serves as the building block for fatty acid synthesis by fatty acid synthase Lastly fatty acids and glycerol are combined to form triacylglycerols which are packaged into VLDL particles in the liver and transported to the adipose tissue where they are stored in lipid droplets This series of enzymatic reactions linking glycolysis the citrate shuttle and fatty acid synthesis explains why eating too many bagels or sucking on too many Jolly Ranchers can result in an increase in total body fat despite consumption of these nonfat carbohydraterich foods The fatty acid 3 oxidation pathway in mitochondria The degradation of fatty acids in animal cells requires enzymatic reactions that occur inside mitochondria as first described by Eugene Kennedy and Albert Lehninger in the late 1940s Subsequent work showed that fatty acids need to be activated by coenzyme A on the cytosolic side ofthe outer mitochondrial membrane and then transported into the mitochondrial matrix by a specific carrier system Fatty acids stored in adipose cells are released into the blood in response to hormone signaling by activation of cellular lipases which cleave stored triacylglycerides The 4 of 9 pages Bioc 460 Dr Miesfeld Fall 2008 fatty acids provide a rich source of energy for tissues throughout the M cquot c c gt body when glycogen stores have o igt o igt o i o ATP been depleted especially during 0 o 39039 endurance exercise and dieting 39 I Figure 6 shows the two step TKO Fatty ac39d fatty acylCoA reaction catalyzed by my WM medium chain fatty acyl CoA synthetase synthetase In the first step the o carboxylate ion of the fatty acid cquot c CEHLO attacks a phosphate in ATP to form 39O li O li O39 R C CL Fatty acyadenyate an acyladenylate intermediate and o o r 0 enzymebound release pyrophosphate PPi which PVV Ph 5Phate is quickly hydrolyzed by the enzyme inorganic fattysjj g j e AMP inorganic pyrophosphatase to quotV39 quot Pquota e 0 form 2 P In the second step of the 2p R Fatty acyl CoA fatty acyl CoA synthetase reaction Y u the palmitoyladenylate intermediate AG 19 kJmol AG 15 kJmol is attacked by the thiol group of CoA lf rthetw 395tep Pmcessl to form the thioester palmitoylCoA product and release AMP As with other reactions we have seen involving PPi the rapid removal of PP as a product of the fatty acyladenylation reaction serves to pull the reaction to the right making it even more favorable Remember to count this reaction as requiring 2 ATP since it requires two rounds of nucleoside kinase 1 ATP each to convert AMP back into ATP The fatty acylCoA products of the fatty acyl CoA synthetase reaction have two fates If the energy charge of the cell is low then they will be imported into the mitochondrial matrix by the carnitine transport cycle and degraded by the fatty acid oxidation reactions to yield acetyl CoA FADH2 and NADH However if the energy charge is high and fatty acid synthesis is favored then mitochondrial import of fatty acylCoA is inhibited and the fatty acylCoA molecule is used instead for triacylglycerol or membrane lipid synthesis in the cytosol Figure 7 illustrates the carnitine transport cycle which involves the function of three proteins and a molecular tag called carnitine In the first reaction carnitine acyltransferase I which is located in the outer mitochondrial membrane replaces the CoA moiety with carnitine to form fatty acyl carnitine which is translocated Figure 7 Cnrnitine lilk llLlllS 39l39th39 ll 0 l l SlOA In termembrano space 39nmitim39 39 39 urmtimv quot oASII Carnitim Yarnitim ucyltmnsloruse I Matrix 5 of 9 pages across the inner mitochondrial membrane The carnitine translocating protein is an antiporter that exchanges a fatty acyl carnitine molecule for a carnitine Once inside the mitochondrial matrix fatty acyl carnitine is converted back to fatty acyl 00A in a reaction catalyzed by carnitine acyltransferase releasing the carnitine so that it can be shuttled back across the inner mitochondrial membrane Once the electronrich carbons of fatty acids are moved into the mitochondrial matrix their high energy redox potential is traded in for a substantial payout of ATP figure g This energy conversion process of fatty acid gt ATP involves oxidation of fatty acids by sequential degradation of 02 units leading to the generation FADHz NADH and acetyl 00A The subsequent oxidation of these reaction products by the citrate cycle and oxidative phosphorylation generates large amounts of ATP Figure 9 illustrates the 3 oxidation pathway used to degrade the C16 fatty acid palmitate The floxidation pathway is so named because the sequential 02 cleavage reaction thiolysis occurs at the 5 carbon of the fatty acid thereby releasing the 01 carboxyl carbon and a carbon as the acetate component of acetyl CoA In the first of four reactions the enzyme acyl CoA dehydrogenase catalyzes a dehydrogenation reaction oxidation that introduces a trans CC bond between the a and 5 carbons ofthe fatty acylCoA molecule using a mechanism that reduces an enzyme bound FAD to form FADHZ Mitochondria actually contain three isozymes of acyl CoA dehydrogenase which differ in their specificity for hydrocarbon chains of different lengths These are referred to as long chain 012 to 013 medium chain C4 to 014 and short chain C4 to Ca acyl CoA dehydrogenases The second reaction in the 5 oxidation pathway is a hydration step catalyzed by the enzyme enoyl CoA hydratase that adds H20 across the 00 bond to convert transAzenoyl CoA to 3L hydroxyacylCoA The third reaction is another dehydrogenation oxidation step in which the enzyme 3 hydroxyacylCoA dehydrogenase removes an electron pair from the substrate and donates it to NAD to form NADH Finally coenzyme A is used in thioysis reaction catalyzed by the enzyme acyl CoA acetyltransferase also called thiolase that releases a molecule of acetyl CoA and in the process results in the formation of an fatty acyl CoA product that is two carbons shorter than the starting substrate These four reactions together convert palmitoyl CoA C16 into myristoylCoA 014 and in the process generate l FADHZ 1 NADH and l acetyl 00A The myristoyl CoA product becomes the substrate for another Bioc 460 Dr Miesfeld Fall 2008 Figure 8 Stage 1 H3 4112 L39 u i10xidmiun 8 AcctylCoA g Citric acid cycle 911 lt G3902 Stage 2 Y 7 sing I NADH FADquot quot 211 og Respiratory ieluclrnn lmnsl39erl chain an ADP 7 9 Figure 9 J r C I 6 R CH CH 2 CH2 C SVC0A PalmitoyleCoA acyeroA FA dehydrogenaxe FAD z i R CHz C 5COA I l 2 H o trans A enoyl0A 2 hydralase OH EnoyLCoA R C H2 li CH2 75420 H o LBHydroxy acylCoA r1ydrnxyaylruA AD dehydrogenase NADH W R C Hz C CHZ C SCOA I KetnacylCOA o acylCM EDASH arelyltrauslerase Khinlase C14 R CHz SCaA Hg li SCDA o 0 CM AcyeroA myristoylCOM Amyl on Bioc 460 Dr Miesfeld Fall 2008 round of 5 oxidation resulting in the production of one more molecule of FADH2 NADH and acetyl 00A The complete oxidation of palmitoylCoA Cm requires seven rounds of the 5 oxidation pathway to convert one molecule of palmitoyl CoA into eight molecules of acetyl CoA in a net reaction that can be written as PamitoyCoA 7 00A 7 FAD 7 NAD 7 H20 gt 8 acetyl CoA 7 FADH2 7 NADH 7 H We are now ready to tally up the net ATP yield from cashing in the redox potential of palmitate using the 5 oxidation pathway As shown in gure 10 after seven rounds of 5 oxidation palmitoylCoA yields 8 acetyl 00A 7 NADH and 7 FADH2 The oxidation of M acetyl CoA by the citrate cycle then 8 acetyl CoA generates 24 NADH 8 FADH2 and 8 l l GTP ATP Finally the combined acewl acetyl acetyl acetyl acetyl acetyl acetyl acetyl reactions of the electron transport C A C A 6 quot C A C A CDA C A C system and oxidative phosphorylation l l l l l l l converts these 31 NADH into 775 02 7 02 7 02 7 02 7 02 7 C2 7 02 7 02 ATP 31 x25 ATP and the 15 l l l l l are Converted into NADH NADH NADH NADH NADH NADH NADH FADH2 FADH2 FADH2 FADH2 FADH2 FADH2 FADHQ 15 x 15 ATP to give a subtotal of 100 ATP After subtracting the 2 ATP 7 NADH required for fatty acyl CoA activation AMP gt PP and adding the 8 ATP 7 FADH2 obtained from eight turns of the citrate cycle you receive a total payout of 106 ATP To appreciate the increased energy yield from fatty acid oxidation as compared to that of glucose oxidation consider that the oxidation of stearate in muscle cells a fully saturated Cm fatty acid yields 120 ATP using the same bookkeeping methods for ATP energy exchange In contrast the complete oxidation of three molecules of glucose 3 x CE Cm generates only 90 ATP or 96 ATP in liver cells The increased energy yield of 33 12090 133 is due to the increased number of electrons available in stearate for donation to the electron transport system stearate is a saturated fatty acid and more highly reduced than glucose When you take into account the fact that the fatty acids in triacylglycerols are hydrophobic and not as hydrated as glucose in glycogen it is easy to see why evolution exploited the energy storage properties of lipids over carbohydrates Besides the payout of ATP that comes from fatty acid oxidation another bene t is the generation of H20 that occurs when 02 is reduced by the final reaction in the electron transport system as well as the formation of H20 in the ATP synthesis reaction of oxidative phosphorylation as shown in the three reactions below 2NADH2H02 gt 2HZO 2 FADH2 02 gt 2 H20 ADP P04Z39 gt ATP H20 The water production that accompanies fatty oxidation bene ts animals that live in dry climates where liquid water is scarce for example the desert kangaroo rat and Arabian camel Large 7 of9 pages Bloc 460 Dr Miesfeld Fall 2008 animals that hibernate over the winter like the Alaskan brown bear also take advantage of fatty acid oxidation in order to M replace H2O that is lost by respiration Fatty acid oxidation of NW palmitate yields 46 H20 molecules generated by the WWW H oxidation of 31 NADH and 15 FADH2 in the electron transport system and 106 H2O molecules formed by the synthesis of 106 WWW H ATP by the ATP synthase reaction By subtracting the 16 H2O 39 molecules required by the citrate cycle 2 H2O for every acetyl CoA oxidized and the 7 H2O molecules used during 5 oxidation the oxidation of 1 mole of palmitate yields 129 moles of H20 152 23 129 This works out to be an amazing 9 milliliters of H20 that are generated from the complete oxidation ofjust1 gram of palmitate Ketogenesis is a salvage pathway for acetyl CoA Kelogznesia When carbohydrate sources are limited due to starvation or when glucose homeostasis is defective as is the case in diabetes ongoing 5 oxidation in liver cell mitochondria results in the buildup of excess acetyl CoA This occurs because flux through the citrate cycle is diminished due to the depletion of oxaloacetate which is siphoned away from the citrate cycle to produce pyruvate for gluconeogenesis Ketogenesis is a process in liver cell mitochondria that takes the excess acetyl CoA and converts it to acetoacetate and D hydroxybutyrate two energyrich compounds that are sometimes called quotketone bodiesquot for historical reasons figure 11 As shown in figure 12 three mitochondrial reactions are required to convert two acetyl CoA molecules into acetoacetate which is then reduced to form DShydroxybutyrate AcylCoA acetyltransferase thiolase is the same enzyme that releases one molecule of acetyl CoA in reaction 4 ofthe 5 oxidation pathway however in this case the reaction is driven toward condensation by the high concentration of acetyl CoA in the mitochondria under ketogenic conditions In the next step the enzyme HMGCoA synthase adds another acetyl CoA group to form the intermediate 5hydroxy5 methylglutarylCoA abbreviated as HMGCoA and then the enzyme HMGCoA lyase removes one of the original acetyl CoA groups to yield acetoacetate Acetoacetate and DShydroxybutyrate are exported from the liver and used by other tissues such as skeletal and heart muscle to generate acetyl CoA for energy conversion reactions figure 13 Even the brain which prefers glucose as an energy source can adapt to using ketone bodies as chemical energy Figure 12 0 O CH Ci CH C 3 3 SCoA S CoA 2 AcetylCoA lhiolase CDA75H 0 0 H CH3 c H2 c SCoA ACEKOBCEWIVCOA HMOCoA AcetylCoA H2O synthase CoArSH 0H 0 C CH2 lt CH2 C 0 CH3 SCoA 3HydroxyHmethylglutarylCOA HMG COA HMGCOA lyase AcetyICuA 0C CH III CH 7 3 0 Acelouetale acemacetate NADH nfJhydroxybutyrate decarboxylase H dEhydmgenase C01 NAD OH 0 CH3 C CH3 C CH2 CH CH3 390 Acetone DBHydroxybutyrate Bloc 460 Dr Miesfeld Fall 2008 during times of extreme starvation as described in lecture 40 While ketogenesis is an important survival mechanism that maintains high rates of fatty acid oxidation when carbohydrates stores are depleted it can also lead to pathological conditions if acetoacetate and DShydroxybutyrate levels in the blood get too high Acidosis is a condition referring to low blood pH which can occur when ketogenesis produces more acetoacetate and DS hydroxybutyrate than what can be utilized by the peripheral tissues these are both carboxylic acids In patients with undiagnosed diabetes which is a metabolic form of carbohydrate quotstarvationquot elevated concentrations of acetoacetate and DShydroxybutyrate in the blood and urine can be several orders of magnitude higher than normal causing nausea vomiting and stomach pain Moreover these individuals also have high levels of acetone in their blood which can be detected on their breath as a fruity odor Acetone is a spontaneous breakdown product of acetoacetate decarboxylation or is formed by enzymatic cleavage of acetoacetate by the enzyme acetoacetate decarboxylase figure 12 The smell of acetone along with the other debilitating symptoms have been known to tragically mislead law officers into thinking these severe cases of diabetes were the result of excess alcohol consumption Ketogenesis is also a hallmark of fasting in which glycogen stores are depleted and energy is derived almost entirely from fatty acid degradation figure 14 This is also true of many low carbohydrate diets that include higher than normal levels of fats as a substitute for bread fruit and W starchy vegetables rice beans potatoes Although there Ketqne Production by Liver During are numerous drawbacks to the extreme versions of these Fawng C dquot39 quot5 Kems39s low carbohydratehigh fat diets there is metabolic logic to why m ng sme a carbohydratedeficient diet will result in a significant decrease in body fat composition due to increased rates of fatty acid oxidation and ketogenesis Pancreas 1x Decreased increased Insulin 39 glucagcn 39 Figure 13 H CHa CI CHz C D Hydroxybutyrate FMS H o J NAB J u prhydroxybutyrate F u a dehydrogenase mm H Jig1 0 CHg C CHz C Acetoacetate leer 0 r M 7 7 3 keloacyl0A 5 quotquot quot W Converted 30 y r quot t k t W transferase a Hes Succlnate ii 909 Ketogenesis o CH3 C CH2 C AcetoacetyICOA Increased ketone production SCoA CoA SH thialase CH 3 C CH3 C SCOA SCOA 2 AcetyICoA Blood vessel 9 of 9 pages
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