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232 / CHAPTER 27neogenesis. Those amino acids that give rise to acetyl-CoA are classified as ketogenic because in the starvingstate much of the acetyl-CoA will be used for synthesisof ketone bodies in the liver.A SUPPLY OF METABOLIC FUELSIS PROVIDED IN BOTH THE FED& STARVING STATES(Figure 27–1)Glucose Is Always Required by the CentralNervous System & ErythrocytesErythrocytes lack mitochondria and hence are whollyreliant on glycolysis and the pentose phosphate pathway.The brain can metabolize ketone bodies to meetabout 20% of its energy requirements; the remaindermust be supplied by glucose. The metabolic changesthat occur in starvation are the consequences of theneed to preserve glucose and the limited reserves ofglycogen in liver for use by the brain and erythrocytesand to ensure the provision of alternative fuels for othertissues. The fetus and synthesis of lactose in milk alsorequire a significant amount of glucose.In the Fed State, Metabolic FuelReserves Are Laid DownFor several hours after a meal, while the products of digestionare being absorbed, there is an abundant supplyof metabolic fuels. Under these conditions, glucose isthe major fuel for oxidation in most tissues; this is observedas an increase in the respiratory quotient (theratio of carbon dioxide produced to oxygen consumed)from about 0.8 in the starved state to near 1 (Table27–1).Glucose uptake into muscle and adipose tissue iscontrolled by insulin, which is secreted by the B isletcells of the pancreas in response to an increased concentrationof glucose in the portal blood. An early responseto insulin in muscle and adipose tissue is the migrationof glucose transporter vesicles to the cell surface, exposingactive glucose transporters (GLUT 4). These insulin-sensitivetissues will only take up glucose from theblood stream to any significant extent in the presence ofthe hormone. As insulin secretion falls in the starvedstate, so the transporters are internalized again, reducingglucose uptake.The uptake of glucose into the liver is independentof insulin, but liver has an isoenzyme of hexokinase(glucokinase) with a high K m , so that as the concentrationof glucose entering the liver increases, so does therate of synthesis of glucose 6-phosphate. This is in excessof the liver’s requirement for energy and is usedmainly for synthesis of glycogen. In both liver andskeletal muscle, insulin acts to stimulate glycogen synthaseand inhibit glycogen phosphorylase. Some of theglucose entering the liver may also be used for lipogenesisand synthesis of triacylglycerol. In adipose tissue, insulinstimulates glucose uptake, its conversion to fattyacids, and their esterification; and inhibits intracellularlipolysis and the release of free fatty acids.The products of lipid digestion enter the circulationas triacylglycerol-rich chylomicrons (Chapter 25). Inadipose tissue and skeletal muscle, lipoprotein lipase isactivated in response to insulin; the resultant free fattyacids are largely taken up to form triacylglycerol reserves,while the glycerol remains in the blood streamand is taken up by the liver and used for glycogen synthesisor lipogenesis. Free fatty acids remaining in theblood stream are taken up by the liver and reesterified.The lipid-depleted chylomicron remnants are alsocleared by the liver, and surplus liver triacylglycerol—including that from lipogenesis—is exported in verylow density lipoprotein.Under normal feeding patterns the rate of tissueprotein catabolism is more or less constant throughoutthe day; it is only in cachexia that there is an increasedrate of protein catabolism. There is net protein catabolismin the postabsorptive phase of the feeding cycleand net protein synthesis in the absorptive phase, whenthe rate of synthesis increases by about 20–25%. Theincreased rate of protein synthesis is, again, a responseto insulin action. Protein synthesis is an energy-expensiveprocess, accounting for up to almost 20% of energyexpenditure in the fed state, when there is an amplesupply of amino acids from the diet, but under 9% inthe starved state.Metabolic Fuel Reserves Are Mobilizedin the Starving StateThere is a small fall in plasma glucose upon starvation,then little change as starvation progresses (Table 27–2;Figure 27–2). Plasma free fatty acids increase withonset of starvation but then plateau. There is an initialdelay in ketone body production, but as starvation progressesthe plasma concentration of ketone bodies increasesmarkedly.In the postabsorptive state, as the concentration ofglucose in the portal blood falls, so insulin secretion decreases,resulting in skeletal muscle and adipose tissuetaking up less glucose. The increase in secretion ofglucagon from the A cells of the pancreas inhibitsglycogen synthase and activates glycogen phosphorylasein liver. The resulting glucose 6-phosphate in liver is
INTEGRATION OF METABOLISM—THE PROVISION OF METABOLIC FUELS / 233Glucose 6-phosphateAcyl-CoAGlycerol 3-phosphateADIPOSETISSUETRIACYLGLYCEROL (TG)cAMPFFAGlycerolEXTRAHEPATICTISSUE (eg,heart muscle)FFALPLGlycerolBLOODGlycerolOxidationLPLFFAFFAChylomicronsTG(lipoproteins)GASTRO-INTESTINALTRACTGlucoseVLDLExtraglucosedrain (eg,diabetes,pregnancy,lactation)GlucoseKetone bodiesFFATGLIVERGlucoseAcyl-CoAGlycerol 3-phosphateAcetyl-CoACitricacidcycle2CO 2Amino acids,lactateGluconeogenesisGlucose 6-phosphateGlycogenFigure 27–1. Metabolic interrelationships between adipose tissue, the liver, and extrahepatictissues. In extrahepatic tissues such as heart, metabolic fuels are oxidized in the following order ofpreference: (1) ketone bodies, (2) fatty acids, (3) glucose. (LPL, lipoprotein lipase; FFA, free fattyacids; VLDL, very low density lipoproteins.)
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a LANGE medical bookHarper’sIllus
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AuthorsDavid A. Bender, PhDSub-Dean
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x / PREFACE• The chapter on plasm
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iv / CONTENTS14. Lipids of Physiolo
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vi / CONTENTSSECTION VI. SPECIAL TO
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4 / CHAPTER 1in early 2001. It is a
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6 / CHAPTER 2H2eCH 3CH 2OHOHFigure
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WATER & pH / 9+ −[ H ][ OH ]−16
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12 / CHAPTER 2meq of alkali added p
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SECTION IStructures & Functionsof P
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16 / CHAPTER 3Table 3-1.L-α-Amino
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18 / CHAPTER 3pK a Values Vary With
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20 / CHAPTER 3121°OC117°122°120
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22 / CHAPTER 4RCFigure 4-1. Compone
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O24 / CHAPTER 4aliphatic polymers 3
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26 / CHAPTER 4NHOR′HNONH 2Phenyli
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28 / CHAPTER 4GENOMICS ENABLES PROT
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Proteins: Higher Orders of Structur
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32 / CHAPTER 50.54-nm pitch(3.6 res
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34 / CHAPTER 5COOHHHC αCHNHHNOC α
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36 / CHAPTER 5sures the absorbance
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38 / CHAPTER 5to a particular organ
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Proteins: Myoglobin & Hemoglobin 6V
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42 / CHAPTER 6Percent saturation100
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44 / CHAPTER 6T structureα 1 α 2O
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46 / CHAPTER 6Adaptation to High Al
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48 / CHAPTER 6Manning JM et al: Nor
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50 / CHAPTER 7132 2Enzyme site14Sub
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52 / CHAPTER 7independent of the co
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54 / CHAPTER 712OCAsp 102OAsp 102HO
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56 / CHAPTER 7NAD(P) + -Dependent D
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58 / CHAPTER 7+ -(Lactate)SH 2LACTA
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Enzymes: Kinetics 8Victor W. Rodwel
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62 / CHAPTER 8that anything which i
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64 / CHAPTER 8Hydrogen Ion Concentr
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66 / CHAPTER 8invertfactorand simpl
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68 / CHAPTER 8only one methylene ca
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70 / CHAPTER 8Increasing[S 2 ]S 11a
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Enzymes: Regulation of Activities 9
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74 / CHAPTER 9influenced both by ch
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76 / CHAPTER 9without affecting the
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78 / CHAPTER 9accounts for the freq
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SECTION IIBioenergetics & the Metab
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82 / CHAPTER 10Figure 10-4. Adenosi
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84 / CHAPTER 10(1) Glucose+P i →
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Biologic Oxidation 11Peter A. Mayes
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88 / CHAPTER 11H 3 CRNNOH 3 CRNHNOH
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90 / CHAPTER 11Amine oxidase, etcNA
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The Respiratory Chain &Oxidative Ph
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94 / CHAPTER 12AH 2 NAD + FpH 2A Fp
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96 / CHAPTER 12NADHSuccinateComplex
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98 / CHAPTER 12ADP+PiβαβATPγα
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100 / CHAPTER 12OUTERMEMBRANEINNERM
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Carbohydrates ofPhysiologic Signifi
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104 / CHAPTER 13HOCH 2HO HOHHOCH 2H
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106 / CHAPTER 13CH 2 OHCH 2 OHCOCH
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O108 / CHAPTER 136HOCH 2O6HOCH 2O4
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110 / CHAPTER 13Figure 13-15.contai
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112 / CHAPTER 1418:1;9 or ∆ 9 18:
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H114 / CHAPTER 14OCOO -more unsatur
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116 / CHAPTER 14Lysophospholipids A
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118 / CHAPTER 14“Chair” form“
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120 / CHAPTER 14RH R• R• ROO•
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Overview of Metabolism 15Peter A. M
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124 / CHAPTER 15(2) It is the precu
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126 / CHAPTER 15FFAGlucosei sl y si
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128 / CHAPTER 15enzyme-catalyzed re
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The Citric Acid Cycle:The Catabolis
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HO CH COO -CH 2 COO -L-MalateMALATE
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134 / CHAPTER 16HydroxyprolineSerin
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Glycolysis & the Oxidationof Pyruva
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GlycogenGlucose 1-phosphateHEXOKINA
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140 / CHAPTER 17lactate and oxidize
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142 / CHAPTER 17[ Acetyl-CoA ][ CoA
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144 / CHAPTER 17Boiteux A, Hess B:
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146 / CHAPTER 18Glycogen(1→4 and
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148 / CHAPTER 18PHOSPHORYLASEGLUCAN
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150 / CHAPTER 18Epinephrineβ Recep
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152 / CHAPTER 18Table 18-2. Glycoge
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PiGLUCOSE-6-PHOSPHATASEH 2 OGlucose
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156 / CHAPTER 19Table 19-1. Regulat
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158 / CHAPTER 19GLUCONEOGENESISP iA
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160 / CHAPTER 19Table 19-2. Glucose
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162 / CHAPTER 19due to hyperactivit
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164 / CHAPTER 20Glucose 6-phosphate
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166 / CHAPTER 20unit comprising car
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168 / CHAPTER 20H *CHHOHHCCCCOHOHHO
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170 / CHAPTER 20AGalactoseGlycogenG
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172 / CHAPTER 20inhibits the activi
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174 / CHAPTER 21CH 3 CO S CoAAcetyl
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176 / CHAPTER 21acids having an odd
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178 / CHAPTER 21crose is fed instea
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Oxidation of Fatty Acids:Ketogenesi
Page 192 and 193: 182 / CHAPTER 221CoAO3 2R CH2 CH2 C
Page 194 and 195: 184 / CHAPTER 22CO 2OCH 3 C CH 2 CO
Page 196 and 197: 186 / CHAPTER 22In extrahepatic tis
Page 198 and 199: 188 / CHAPTER 22GlucoseBLOODFFAVLDL
Page 200 and 201: Metabolism of Unsaturated FattyAcid
Page 202 and 203: 192 / CHAPTER 2318O12 9C S CoALinol
Page 204 and 205: 194 / CHAPTER 23COOHO O Arachidonat
Page 206 and 207: 196 / CHAPTER 23hepatorenal syndrom
Page 208 and 209: ATPADPNAD + NADH + H +H 2 COHH 2 CO
Page 210 and 211: 200 / CHAPTER 24H 2 COHO CH 2 C O P
Page 212 and 213: 202 / CHAPTER 24CH 3O(CH 2 ) 14 C S
Page 214 and 215: 204 / CHAPTER 24SUMMARY• Triacylg
Page 216 and 217: 206 / CHAPTER 25Table 25-1. Composi
Page 218 and 219: •••208 / CHAPTER 25AIntestina
Page 220 and 221: 210 / CHAPTER 25NascentVLDLB-100ELD
Page 222 and 223: 212 / CHAPTER 25the fed state rathe
Page 224 and 225: 214 / CHAPTER 25and may account for
Page 226 and 227: 216 / CHAPTER 25Epinephrine,norepin
Page 228 and 229: 218 / CHAPTER 25• Apolipoproteins
Page 230 and 231: 220 / CHAPTER 26OCH 3 C S CoA2 Acet
Page 232 and 233: 222 / CHAPTER 26OCH 3CH 3CH 3CSCoA-
Page 234 and 235: 224 / CHAPTER 26CELL MEMBRANELDL (a
Page 236 and 237: 226 / CHAPTER 2612 17Vitamin CNADP
Page 238 and 239: 228 / CHAPTER 26lesterol into the c
Page 240 and 241: 230 / CHAPTER 26Russell DW: Cholest
Page 244 and 245: 234 / CHAPTER 27Table 27-1. Energy
Page 246 and 247: 236 / CHAPTER 27CLINICAL ASPECTSIn
Page 248 and 249: 238 / CHAPTER 28O- O O-NH+ 3- O O-O
Page 250 and 251: 240 / CHAPTER 28CH 2 CH COO -+ NH 3
Page 252 and 253: Catabolism of Proteins& of Amino Ac
Page 254 and 255: 244 / CHAPTER 29of amino groups to
Page 256 and 257: 246 / CHAPTER 29CO 22Mg-ATPN-Acetyl
Page 258 and 259: 248 / CHAPTER 29Argininosuccinicaci
Page 260 and 261: 250 / CHAPTER 30CONH 2H 2 O NH 4+CO
Page 262 and 263: 252 / CHAPTER 30H 2 CNH 3+CHCO -H 4
Page 264 and 265: O -254+NH 3 O2CH O - 1 α-KG 1 GluC
Page 266 and 267: OOCCH 2CH 2COCO -H 2 OOCCH 2CH 2COC
Page 268 and 269: 258 / CHAPTER 30HOHONH 2OCNH 3+NCH
Page 270 and 271: 260 / CHAPTER 30CH 3NH 3+NH 3+NH 3+
Page 272 and 273: 262 / CHAPTER 30OOH 2 C CC S CoACH
Page 274 and 275: Conversion of Amino Acidsto Special
Page 276 and 277: 266 / CHAPTER 31PROTEINSNITRIC OXID
Page 278 and 279: +H 2 NHNHCNH 2NHCHCH 2CH 2 + H3 N C
Page 280 and 281: Porphyrins & Bile Pigments 32Robert
Page 282 and 283: 272 / CHAPTER 32APAPPAAPAPAPUroporp
Page 284 and 285: 274 / CHAPTER 32AHOOCH 2 CH 2 CNH 2
Page 286 and 287: 276 / CHAPTER 32HemoproteinsProtein
Page 288 and 289: 278 / CHAPTER 32indicated in Figure
Page 290 and 291: 280 / CHAPTER 32Bilirubin formed in
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282 / CHAPTER 32MH 2 CMINHEOHOHMMH
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284 / CHAPTER 32Table 32-3. Laborat
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SECTION IVStructure, Function, & Re
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288 / CHAPTER 33Table 33-1. Bases,
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290 / CHAPTER 33NNH 2NNNTable 33-2.
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292 / CHAPTER 33Pu/Py R O P O P OO
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294 / CHAPTER 34N 10 -Formyltetrahy
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296 / CHAPTER 34HNO-OOCNCHC COO - -
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298 / CHAPTER 34CO 2 + Glutamine +
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300 / CHAPTER 34OTHER DISORDERS OFP
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302 / CHAPTER 34REFERENCESBenkovic
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304 / CHAPTER 35O5′CH 2NNGNNHNH 2
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306 / CHAPTER 35dures allow for ver
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308 / CHAPTER 35O5′CH 2NNGNNHNH 2
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310 / CHAPTER 355′3′DNA3′5′
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312 / CHAPTER 35Region of hydrogenb
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DNA Organization, Replication,& Rep
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316 / CHAPTER 36understood. It is p
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318 / CHAPTER 36more extended chrom
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320 / CHAPTER 361 2 3 4 56 7 8 9 10
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322 / CHAPTER 36spersed repeats, in
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324 / CHAPTER 36Gγ Aγ δ βδ βG
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326 / CHAPTER 36contains an intersp
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328 / CHAPTER 36Table 36-5. Classes
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330 / CHAPTER 36with the other stra
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332 / CHAPTER 36lizing proteins bin
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334 / CHAPTER 36Improper spindledet
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336 / CHAPTER 36Table 36-9. Mechani
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338 / CHAPTER 363′5′3′5′3
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340 / CHAPTER 36Marians KJ: Prokary
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342 / CHAPTER 37Table 37-1. Classes
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344 / CHAPTER 37cule from the 5′
Page 356 and 357:
346 / CHAPTER 37coordinately regula
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348 / CHAPTER 37site (from −3 to
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350 / CHAPTER 37Finally, this newly
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352 / CHAPTER 37activators are not
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354 / CHAPTER 37is accomplished by
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356 / CHAPTER 37(the histones are m
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Protein Synthesis & theGenetic Code
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360 / CHAPTER 38Table 38-2. Feature
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362 / CHAPTER 38Hemoglobin Illustra
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364 / CHAPTER 38NormalWild typemRNA
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Ternary complexformationFormation o
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368 / CHAPTER 38GTPG m TP—5′+P
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370 / CHAPTER 38Table 38-3. Evidenc
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372 / CHAPTER 38molecules. This dif
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Regulation of Gene Expression 39Dar
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376 / CHAPTER 39be regarded as a on
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378 / CHAPTER 39above sequence). At
Page 390 and 391:
380 / CHAPTER 39AGene for repressor
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ProphageO R 3O R 2 O R 1RNA polymer
Page 394 and 395:
384 / CHAPTER 39promoter dictates w
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386 / CHAPTER 39HMG PRDIV HMG PRDI-
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388 / CHAPTER 395′HREAREPORTER GE
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390 / CHAPTER 39protein of E coli),
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392 / CHAPTER 39GAL4 +1ActiveAUASGA
Page 404 and 405:
394 / CHAPTER 39mouse amylase and m
Page 406 and 407:
Molecular Genetics, RecombinantDNA,
Page 408 and 409:
398 / CHAPTER 40DNA 5′Regulatoryr
Page 410 and 411:
400 / CHAPTER 40A. Sticky or stagge
Page 412 and 413:
402 / CHAPTER 40Table 40-4. Cloning
Page 414 and 415:
404 / CHAPTER 40Southern Northern W
Page 416 and 417:
406 / CHAPTER 40STARTCYCLE 1CYCLE 2
Page 418 and 419:
408 / CHAPTER 40∋Gγ Aγ Ψβ δ
Page 420 and 421:
410 / CHAPTER 40A. MstII restrictio
Page 422 and 423:
412 / CHAPTER 40percentage of genes
Page 424 and 425:
414 / CHAPTER 40Primosome: The mobi
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416 / CHAPTER 41products, and toxic
Page 428 and 429:
418 / CHAPTER 41hydrophobic regions
Page 430 and 431:
420 / CHAPTER 41Table 41-2. Enzymat
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422 / CHAPTER 41attack by nucleases
Page 434 and 435:
424 / CHAPTER 41Transportedmolecule
Page 436 and 437:
426 / CHAPTER 41Table 41-4. Some pr
Page 438 and 439:
428 / CHAPTER 41INSIDEATPADP+P i3 N
Page 440 and 441:
430 / CHAPTER 41broblasts, for exam
Page 442 and 443:
432 / CHAPTER 41Table 41-5. Some di
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The Diversity of theEndocrine Syste
Page 446 and 447:
436 / CHAPTER 42◆❁❁✪✴ ❖
Page 448 and 449:
438 / CHAPTER 42Hormones Are Chemic
Page 450 and 451:
440 / CHAPTER 42HOABCCCDC C CC CCCh
Page 452 and 453:
442 / CHAPTER 42the gonads and acts
Page 454 and 455:
444 / CHAPTER 42OHOH5α-REDUCTASENA
Page 456 and 457:
446 / CHAPTER 42Sunlight7-Dehydroch
Page 458 and 459:
448 / CHAPTER 42FOLLICULAR SPACE WI
Page 460 and 461:
450 / CHAPTER 4220NH 2 -Ala Leu Pro
Page 462 and 463:
452 / CHAPTER 42AngiotensinogenAsp-
Page 464 and 465:
454 / CHAPTER 42Table 42-5. Diversi
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Hormone Action &Signal Transduction
Page 468 and 469:
458 / CHAPTER 43−Cytoplasm−++TR
Page 470 and 471:
460 / CHAPTER 43NNHEEα sGDPγβCNo
Page 472 and 473:
462 / CHAPTER 43Activeadenylylcycla
Page 474 and 475:
464 / CHAPTER 43A number of critica
Page 476 and 477:
466 / CHAPTER 43RECOGNITION(HYPERGL
Page 478 and 479:
468 / CHAPTER 43C. THE NF-B PATHWAY
Page 480 and 481:
470 / CHAPTER 43A/BCDEFNAF-1DBDHing
Page 482 and 483:
472 / CHAPTER 43Table 43-5. Nuclear
Page 484 and 485:
SECTION VISpecial TopicsNutrition,
Page 486 and 487:
INTESTINALLUMEN1AcylPANCREATICAcylL
Page 488 and 489:
478 / CHAPTER 44Iron Absorption Is
Page 490 and 491:
480 / CHAPTER 44growing children ar
Page 492 and 493:
482 / CHAPTER 45Table 45-1. The vit
Page 494 and 495:
484 / CHAPTER 45H 3 CH 3 CH 3 CH 3
Page 496 and 497:
486 / CHAPTER 45tration of calcium.
Page 498 and 499:
488 / CHAPTER 45OCH 3HO 3Phylloquin
Page 500 and 501:
490 / CHAPTER 45FMN. The main dieta
Page 502 and 503:
492 / CHAPTER 45H 3 CH 2 NCOCH 2 CH
Page 504 and 505:
494 / CHAPTER 45droxymethyltransfer
Page 506 and 507:
496 / CHAPTER 45CH 2 OHCH 2 OHCH 2
Page 508 and 509:
Intracellular Traffic & Sortingof P
Page 510 and 511:
Plasma membraneCytosolEarlyendosome
Page 512 and 513:
502 / CHAPTER 4612GTP3GDPTargeting
Page 514 and 515:
504 / CHAPTER 46at their amino term
Page 516 and 517:
506 / CHAPTER 46NNNCNCCNNEXTRACYTOP
Page 518 and 519:
508 / CHAPTER 46Table 46-4. Some se
Page 520 and 521:
510 / CHAPTER 46Coated3 vesicle4t-S
Page 522 and 523:
512 / CHAPTER 46Membrane proteinExt
Page 524 and 525:
Glycoproteins 47Robert K. Murray, M
Page 526 and 527:
516 / CHAPTER 47Table 47-4. The pri
Page 528 and 529:
518 / CHAPTER 47animal origin are n
Page 530 and 531:
520 / CHAPTER 47NO-glycan chainTand
Page 532 and 533:
522 / CHAPTER 47α2,3 or 2,6Sialic
Page 534 and 535:
524 / CHAPTER 47Man α1,2 GlcNAc P
Page 536 and 537:
526 / CHAPTER 47Table 47-10. Summar
Page 538 and 539:
528 / CHAPTER 47Additional constitu
Page 540 and 541:
530 / CHAPTER 47ABCDBaselineRolling
Page 542 and 543:
532 / CHAPTER 47Mutations in DNAMut
Page 544 and 545:
534 / CHAPTER 47• The structures
Page 546 and 547:
536 / CHAPTER 48Table 48-1. Types o
Page 548 and 549:
538 / CHAPTER 48this matrix are the
Page 550 and 551:
540 / CHAPTER 48other gene for fibr
Page 552 and 553:
542 / CHAPTER 48other plasma protei
Page 554 and 555:
544 / CHAPTER 48β1,4 β1,3Hyaluron
Page 556 and 557:
546 / CHAPTER 48Table 48-7. Biochem
Page 558 and 559:
548 / CHAPTER 48(see above), where
Page 560 and 561:
550 / CHAPTER 48Blood capillaryNucl
Page 562 and 563:
552 / CHAPTER 48in structurally abn
Page 564 and 565:
554 / CHAPTER 48mal trunk size, mac
Page 566 and 567:
Muscle & the Cytoskeleton 49Robert
Page 568 and 569:
558 / CHAPTER 49H bandA. ExtendedI
Page 570 and 571:
560 / CHAPTER 49Myosins constitute
Page 572 and 573:
562 / CHAPTER 49123Thick filamentLM
Page 574 and 575:
564 / CHAPTER 49Depolarization of n
Page 576 and 577:
566 / CHAPTER 49Table 49-2. Some ot
Page 578 and 579:
568 / CHAPTER 49Table 49-3. Some di
Page 580 and 581:
570 / CHAPTER 49cardiomyopathy. In
Page 582 and 583:
572 / CHAPTER 49Table 49-7. Actin-m
Page 584 and 585:
574 / CHAPTER 49Table 49-8. Summary
Page 586 and 587:
576 / CHAPTER 49carbonate) loading,
Page 588 and 589:
578 / CHAPTER 49disappearing during
Page 590 and 591:
Plasma Proteins & Immunoglobulins 5
Page 592 and 593:
582 / CHAPTER 50AC+ -Albumin α 1
Page 594 and 595:
584 / CHAPTER 50tively early in con
Page 596 and 597:
586 / CHAPTER 50the level of the en
Page 598 and 599:
588 / CHAPTER 50Copper Is a Cofacto
Page 600 and 601:
590 / CHAPTER 50disease). In this c
Page 602 and 603:
592 / CHAPTER 50+ H3 N+ H3 NV LFabS
Page 604 and 605:
594 / CHAPTER 50Table 50-8. Major f
Page 606 and 607:
596 / CHAPTER 50Myeloma cellHybrido
Page 608 and 609:
Hemostasis & Thrombosis 51Margaret
Page 610 and 611:
600 / CHAPTER 51Table 51-1. Numeric
Page 612 and 613:
602 / CHAPTER 51PrethrombinCa 2+ Ca
Page 614 and 615:
604 / CHAPTER 51disease because fac
Page 616 and 617:
606 / CHAPTER 51Table 51-3. Compari
Page 618 and 619:
608 / CHAPTER 51dothelial cells, bu
Page 620 and 621:
Page 622 and 623:
Page 624 and 625:
614 / CHAPTER 52Mutations in the ge
Page 626 and 627:
616 / CHAPTER 52Table 52-6. Princip
Page 628 and 629:
618 / CHAPTER 52antibodies. For pur
Page 630 and 631:
620 / CHAPTER 52Table 52-7. Laborat
Page 632 and 633:
622 / CHAPTER 52Table 52-11. Exampl
Page 634 and 635:
624 / CHAPTER 52Table 52-12. Protei
Page 636 and 637:
Metabolism of Xenobiotics 53Robert
Page 638 and 639:
628 / CHAPTER 53smooth endoplasmic
Page 640 and 641:
630 / CHAPTER 53This reaction helps
Page 642 and 643:
632 / CHAPTER 53human genome, a new
Page 644 and 645:
634 / CHAPTER 5420 30 30 20 25cMGen
Page 646 and 647:
636 / CHAPTER 54DETERMINATION OF TH
Page 648 and 649:
638 / CHAPTER 54the proteome), incl
Page 650 and 651:
640 / APPENDIXOffice of Rare Diseas
Page 652 and 653:
IndexNote: Page numbers in bold fac
Page 654 and 655:
INDEX / 645Alpha-amino nitrogen. Se
Page 656 and 657:
INDEX / 647Aromatase enzyme complex
Page 658 and 659:
INDEX / 649Bronze diabetes, 587Brow
Page 660 and 661:
INDEX / 651CFU-E. See Colony-formin
Page 662 and 663:
INDEX / 653immunoglobulin heavy cha
Page 664 and 665:
INDEX / 655Detoxification, 626cytoc
Page 666 and 667:
INDEX / 657EcoRI, 398, 399t, 401fEc
Page 668 and 669:
INDEX / 659Extrinsic pathway of blo
Page 670 and 671:
INDEX / 661∆G F , 61enzymes affec
Page 672 and 673:
INDEX / 663Glutamine analogs, purin
Page 674 and 675:
INDEX / 665Heat, free energy libera
Page 676 and 677:
INDEX / 667Hybridomas, 595-596, 596
Page 678 and 679:
INDEX / 669Intracellular signals, 4
Page 680 and 681:
INDEX / 671Ligand-receptor complex,
Page 682 and 683:
INDEX / 673Melting point, of amino
Page 684 and 685:
INDEX / 675regulation ofactin-based
Page 686 and 687:
INDEX / 677Nucleus (cell), importin
Page 688 and 689:
INDEX / 679Phenylisothiocyanate (Ed
Page 690 and 691:
INDEX / 681Positive regulators, of
Page 692 and 693:
INDEX / 683transport, 454-455, 454t
Page 694 and 695:
INDEX / 685Reversed-phase high-pres
Page 696 and 697:
INDEX / 687Skinessential fatty acid
Page 698 and 699:
INDEX / 689Tertiary structure, 33-3
Page 700 and 701:
INDEX / 691Troponin I, 562Troponin
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INDEX / 693Wilson disease, 432t, 58
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Harpers

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