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Home , Acetoacetic acid

782 CHAPTER2s Lipid Metabolism

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Lipids are extremely important as nutrients and in two compounds are used for energy production in cell membranes.Reserves of stored triglyceridesare the . mobilized as needed for energy production. Fat The brain usually needsglucose, but it adaptsto mobilization is stimulated by epinephrine (adrena- body oxidation in about 2 days.Excess pro- lin). The triglycerides are hydrolyzed into fatty acids duction of ketone body acids leads to ketonemia and glycerol, which enter the bloodstream. In tis- ( in the blood). The ketone bodies sues,free fatty acids are converted to fatty acyl CoA eventually appear in the urine (). Chronic molecules,which are broken donm to aceWlCoA bv overproduction of ketone body acids leads to in the . The acetyl ketone body acidosis() of the blood because CoA may be used for energy production by way of the kidneys cannot supply enough bicarbonateions the citric acid cycle and the electron transport to neutralize the acids. chain. The liver sj,nthesizescholesterol from acetyl Beta oxidation of fatty acids is a good sourceof CoA.The cellular cytoplasmis the site of energy. One molecule of palmitic acid produces synthesis.Too much cholesterol in the blood may enough energy to phosphorylate 129 molecules of cause the formation of atherosclerotic plaque-a ADP to ATP \tVhenAIP is in abundant supply, acetyl buildup of layers of cholesterol and cells on arterial CoAis resynthesizedback to fatty acidsor to choles- walls.The resulting constriction of the blood vessels terol.\Mhen ATP is in short supply and glucoseis not causesharmful effects on circulation; a blockage in available,as in starvation or diabetes,the liver uses the arteries of the heart can cause heart failure. acetyl CoA to make the ketone bodies , B- Blood cholesterolis sometimesheilped by exercise, hydroxybutyric acid, and acetoaceticacid; the latter a low-saturated-fatdiet, or medication.

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Adiposetissue (25.1) spiral (25.3) Ketonemia(25.9) Plaque(25.11) Atherosclerosis(25.1 1) Fatty acyl CoA (25.3) Ketonuria (25.9) Storagefat (25.1) Betaoxidation (25.3) (25.9) Ketosis(25.9) Tissuelipid (25.1) Depotfat (25.1) Ketonebodies (25.8) Mobilization (25.2) Workinglipid (25.1)

ffiH#g*$sHg BodyLipids (sections 25,1,25.21 FattyAcid Metabolism and Storage (Sections 25.5 Draw the structure of a triglyceride that contains 25.t, 25.4,25,5, 25,6, 25,71 stearic,oleic, and linoleic acids. 25.13 \Mherein the cell does fatty acid catabolism occur? 25.6 \A/hatare the products of hydrolysis of the triglyc- 25.14 How is a fatty acid prepared for entry into a mito- eride in Exercise25.5? Name the en4rme that catalyzes chondrion? the process. 25.15 \A/hatis meant by the term beta oxidation? 25.7 Describehow lipids are distributed in body tissues. 25.16 \tVhyis the degradationpathway of fatty acids called 25.8 Discussthe functions of adiposetissue. the fatty acid spirahalher than the fatty acid cycle? 25.9 \Mhat stimulates the hydrolysis of triglycerides? 25.17 The fatty aryl CoA formed from the l0-carbon acid 25.10 Explain the function of serum albumin in fatty capric acid is degradedby beta oxidation to acetyl CoA. acid transport. \Mhat is the yield of (a) acetyl CoA, (b) NADH, and (c) 25.1I \t\trich tissuesprefer glucoseto fatty acids for en- FADH2? ergy production? 25.18 \Mhat is the maximum number of AIP molecules 25.I 2 \A/hatis the causeof lipid storagediseases? that can be produced in the complete oxidation of capric acid to and water? (SeeTable 25.1.) Exercises 781

25.19 'vVhyis acetyl CoA a key compound in the interplay 25.34 Vvhatis the total AIP yield from the complete between fatty acid and carbohydrate metabolism? oxidation of 1 mol of myristic acid, CH.(CH)2CO1}| 25.20 Describe the four fates that await aceM CoA in the to carbon dioxide and water? liver. 25.35 How are fatty acid molecules prepared for trans- 25.21 How does the camel'shump permit it to survive port acrossthe mitochondrial membrane? famine and drought? 25.36 Name and describe the severalconditions that are 25.22 Fxplun why fatty acids are more efficient energy s)'rrrptomsof ketosis. storesthan glycogen. 25.37 Acetoaceticacid and B-hydroxybutyric acid, two of the ketone bodies, are used by the brain, the heart, and KetoneBodies and Diabetes (Sections 25.8,25.9) skeletal muscle as a source of energy.\Mhy do these compoundspresent a seriousproblem in diabetesor 25.23 \A/hatis the difference between starvation and stawation? diabetes? 25.38 \Mherein the cell does (a) fatty acid catabolism 25.24 l//hat are the ketone bodies? take place?(b) fatty acid activation occur? 25.25 How do ketonebodies form? 25.39 How do low blood glucoselevels trigger the mobi- 25.26 Explain why untreated diabetics accumulate large lization offatty acids from adipose tissue? amounts of ketonebodies. 25.40 Explain why the mobilization of fatty acids from 25.27 Define (a) ketonemia, (b) ketonuria, (c) acetone adiposetissue stops when blood glucoselevel rises. breath, and (d) ketosis. 25.41 For each statement, write the number of the cor- 25.28 Describe how untreated diabetes mellitus leads to rect name and the number for the correct structure. coma and death. (a) Aketonebodythat (1) acetoacetylCoA is not used as an energy (2) fatty acyl CoA (3) p-hydroxybutyric Cholesterol(Sections 25.1O, 25.1 l) (b) Producedbyreaction acid 25.29 \Mheredoes cholesterol slmthesistake place?lVhat of a fatty acid with CoA (4) acetyl CoA is usedas "startingmaterial"? (c) Aproductofthe (5) acetone 25.30 Explain why cholesterol slmthesisslows dor,vn hydrolysis in adipose (6) acetoaceticacid when a cell needs energy. tissue (7) a fatty acid (d) Aketone body 25.31 \Mhatis atherosclerosis? that is not really a o 25.32 Explain why an increasedintake of unsaturated ketone (B) CH3(CHilaCSCoA fats is more helpful in reducing plasma cholesterol (e) Reactswith CoA than decreasingdietary cholesterol. to produce two o moleculesof (9) CHSCCHS AdditionalExercises substance(14) (f) One of the ketone oo 25.33 Match the following: bodies ilil (a) beta oxidation (1) ketone body (r0) CH3CCH2CSCoA (g) Intermediate of (b) ketonemia (2) blood acidosis both carbohydrate OH (c) fatty acid slmthesis causedby ketone and lipid metabolism I (d) ketonuria bodies (r1) CH3CHCH2CO2H ,(e) mitochondria (3) synthesizedfrom o (f) cholesterol aceryl CoA (g) epinephrine (4) degradation of (12) CH3CCH2CO2H (h) glycerol fattyacids (13)cH3(cH)ucozH (i) acetone (5) ketonebodies in (j) ketosis blood o (6) enters glycolysis (r4) (7) site of beta oxidation CH3dscoA (B) fatty acid mobi- lization (e)utilizes AIP (10)ketone bodies in urine 784 CHAPTER25 Lipid Metabolism sfiLF-THST{RElfEsW} True/False

l. Working lipids are generallylocalized in muscle 15. In the aerobic catabolism of a molecule of a fatty tissue. acid, a majority of the energy is produced 2. For equal weights, fats are better sourcesof energy (a) directly asAIP in the citric acid cycle. than carbohydrates. (b) from NADH from the fatty acid spiral. 3. Epinephrine stimulates the hydrolysis of glycogen (c) from NADH from the citric acid cycle. and triglycerides. (d) from FADH, from the fatty acid cycle. 4. Once acetyl CoA is in the mitochondria, it is always 16. In the actual oxidation step ofbeta oxidation, (a) used for energy production in the citric acid cycle. an alcoholis oxidizedto an acid. (b) an is oxidized to a ketone. 5. Fatty acids can be converted to carbohydrates (c) an alcohol is oxidized to an through an aceryl CoA intermediate. aldehyde. (d) an aldehyde is oxidized to an acid. - 6. The principal site of is the liver. f 7. Acetyl CoA in the liver may be converted to all the 7. A body with low AIP demand and excessglucose following except responds by making and storing fatty acid molecules. (a) cholesterol. (b) glycogen. 8. The beta oxidation of a molecule of (c) fatryacid. (d) ketonebodies. cH3(cHrl6co2H lB. Efficient energy storageis achievedby (a) convertingfats to glycogen. would yield nine molecules each of aceryl CoA, (b) eliminating all fatty foods from the diet. NADH, andFADHr. (c) converting excessacetyl CoA into stored triglyc- 9. Glucosemetabolism has no effect on the formation erides. ofketone bodies. (d) avoiding the use of AIP in forming storagecom- pounds. 10. The rate of slmthesisof cholesterol increasesas the rate of aceryl CoA oxidation in the citric acid cycle 19. Tay-Sachsdisease is associatedwith increases. (a) a defect in lipid anabolism. (b) the unavailability of complex lipids for use in the brain and liver. (c) a defect in lipid catabolism. MultipleChoice (d) a defect in the processbywhich cholesterol is synthesized. I l. An untreated severediabetic would probably 20. Supposethat you haverft eaten for 5 hours and you experience begin jogging. \iVhich of the following statements (a) acetone breath. (b) glucosuria. aboutyour system is nottrue? (c) ketonemia. (d) allof these. (a) Triglyceridesare being hydrolyzed. 12. \Mhich of the following does not occur in the mito- (b) Glucoseis being changed to glycogen. chondria of liver cells? (c) Fatty acids are being broken dor,rinto acetyl CoA. (a) slmthesisof (d) Cholesterol slmthesisis minimal. (b) beta oxidation 21. A deficiency of glucosein cells (c) citric acid cycle (a) increasesthe rate of beta oxidation of fatty acid. (d) synthesisof cholesterol (b) can be a result of severediabetes. 13. The glycerol produced by the hydrolysis of triglyc- (c) results in the formation of ketone bodies. erides enters the metabolic pathway in (d) all of the above are true. (a) the citric acid cycle. 22. In severediabetic ketosis, (b) oxidative phosphorylation. (a) the concentration of H* eventually drops. (c) glycolysis. (b) oxygen transport byhemoglobin is impaired. (d) the fatty acid spiral. (c) the pH of the blood remains unchanged. 14. Fat tissuein the bodyis (d) the bicarbonate ion concentration increases. (a) an important sourceof bodyheat. 23. Ketone bodies are not utilized as an energy source in (b) also called adipose tissue. the (c) a goodinsulator. (a) brain. (b) Iiver. (d) alloftheabove. (c) heart. (d) skeletal muscles.