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HormonalRegulationandIntegrationofMammalianMetabolismS-2661.PeptideHormoneActivityExplainhowtwopeptidehormonesasstructurallysimilarasoxytocinandvasopressincanhavesuchdifferenteffects(seeFig.23–10).AnswerOxytocinandvasopressinarerecognizedbydifferentreceptors,typicallyfoundindifferentcelltypes.Thesereceptorsarecoupledtodifferentdownstreameffectsintheirtargetcells.2.ATPandPhosphocreatineasSourcesofEnergyforMuscleDuringmusclecontraction,thecon-centrationofphosphocreatineinskeletalmuscledropswhiletheconcentrationofATPremainsfairlyconstant.However,inaclassicexperiment,RobertDaviesfoundthatifhefirsttreatedmusclewith1-fluoro-2,4-dinitrobenzene(p.94),theconcentrationofATPdeclinedrapidlywhiletheconcentrationofphosphocreatineremainedunchangedduringaseriesofcontractions.Suggestanexplanation.AnswerMusclecontractionresultsinanethydrolysisofATP.AlthoughtheamountofATPinmuscleisverysmall,thesupplycanberapidlyreplenishedbyphosphorylgrouptransferfromthephosphocreatinereservoir,catalyzedbycreatinekinase:PhosphocreatineADP34creatineADPBecausethisreactionisrapidrelativetotheuseofATPbymuscle,[ATP]remainsinasteadystate.Theeffectofpretreatmentwithfluoro-2,4-dinitrobenzenesuggeststhatthisisaneffec-tiveinhibitorofcreatinekinase.Underworkingconditions,thesmallamountofmuscleATPisquicklydepletedandcannotbereplenished.3.MetabolismofGlutamateintheBrainBraintissuetakesupglutamatefromtheblood,transformsitintoglutamine,thenreleasesitintotheblood.Whatisaccomplishedbythismetabolicconversion?Howdoesittakeplace?Theamountofglutamineproducedinthebraincanactuallyexceedtheamountofglutamateenteringfromtheblood.Howdoesthisextraglutaminearise?(Hint:youmaywanttoreviewaminoacidcatabolisminChapter18;recallthatNH3isverytoxictothebrain.)AnswerAmmoniaisverytoxictonervoustissue,especiallythebrain.ExcessNH3inbraincellsisremovedbythetransformationofglutamatetoglutamine,catalyzedbyglutaminesyn-thetase.Glutamineisthenexportedtothebloodandtravelstotheliver,whereitistrans-formedtourea.Theadditionalglutamineinthebrainarisesfromtheactionofaminotransferasesthattransferaminogroupsfromaminoacidstoa-ketoglutarate(acitricacidcycleintermediate),formingglutamate,whichisthenconvertedtoglutamine.chapter232608T_ch23sm_S266-S27302/26/200812:03amPageS-266pinnacleOS9:DesktopFolder:WHQY028:4.ProteinsasFuelduringFastingWhenmuscleproteinsarecatabolizedinskeletalmuscleduringafast,whatarethefatesoftheaminoacids?AnswerGlucogenicaminoacidsareusedtomakeglucoseforthebrain;othersareoxidizedinmitochondriaviathecitricacidcycle.5.AbsenceofGlycerolKinaseinAdiposeTissueGlycerol3-phosphateisrequiredforthebiosyn-thesisoftriacylglycerols.Adipocytes,specializedforthesynthesisanddegradationoftriacylglycerols,cannotuseglyceroldirectlybecausetheylackglycerolkinase,whichcatalyzesthereactionGlycerolATP88nglycerol3-phosphateADPHowdoesadiposetissueobtaintheglycerol3-phosphatenecessaryfortriacylglycerolsynthesis?AnswerAdiposetissueconvertsglucosetotheglycolyticintermediatedihydroxyacetonephosphate,whichisreducedtoglycerol3-phosphatebytheNADH-requiringenzymeglycerol3-phosphatedehydrogenase:glycolysisGlucose8888888ndihydroxyacetonephosphateDihydroxyacetonephosphateNADHH34glycerol3-phosphateNAD6.OxygenConsumptionduringExerciseAsedentaryadultconsumesabout0.05LofO2in10sec-onds.Asprinter,runninga100mrace,consumesabout1LofO2in10seconds.Afterfinishingtherace,thesprintercontinuestobreatheatanelevated(butdeclining)rateforsomeminutes,consum-inganextra4LofO2abovetheamountconsumedbythesedentaryindividual.(a)WhydoestheneedforO2increasedramaticallyduringthesprint?(b)WhydoesthedemandforO2remainhighafterthesprintiscompleted?Answer(a)IncreasedmuscleactivityraisesthedemandforATP,whichismetbyincreasedactivityofthecitricacidcycleenzymesandincreasedflowofelectronsthroughtheelectron-transferchain.ThisresultsingreaterO2consumption.(b)Duringthesprint,muscletransformssomeglycogentolactate(anaerobicglycolysis).Afterthesprint,lactateistransportedtotheliver,whereitisconvertedbacktoglucoseandglyco-gen.ThisprocessrequiresATPandthusrequiresO2consumptionabovetherestingrate.7.ThiamineDeficiencyandBrainFunctionIndividualswiththiaminedeficiencyshowsomecharac-teristicneurologicalsignsandsymptoms,includinglossofreflexes,anxiety,andmentalconfusion.Whymightthiaminedeficiencybemanifestedbychangesinbrainfunction?AnswerGlucoseistheprimaryfuelofthebrain,andthebrainisparticularlysensitivetoanychangeintheavailabilityofglucoseforenergyproduction.Akeyreactioninglucosecatabo-lismisthethiaminepyrophosphate–dependentoxidativedecarboxylationofpyruvatetoacetyl-CoA.Thus,athiaminedeficiencyreducestherateofglucosecatabolism.8.PotencyofHormonesUndernormalconditions,thehumanadrenalmedullasecretesepinephrine(C9H13NO3)ataratesufficienttomaintainaconcentrationof1010Mincirculatingblood.Toappreci-atewhatthatconcentrationmeans,calculatethediameterofaroundswimmingpool,withawaterdepthof2.0m,thatwouldbeneededtodissolve1.0g(about1teaspoon)ofepinephrinetoaconcen-trationequaltothatinblood.Chapter23HormonalRegulationandIntegrationofMammalianMetabolismS-2672608T_ch2
本文标题:Lehninger-Principles-of-Biochemistry-习题答案chapter-2
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