Obesity Before Birth: Maternal and prenatal influences on the offspring PDF
Preview Obesity Before Birth: Maternal and prenatal influences on the offspring
OBESITY BEFORE BIRTH ENDOCRINEUPDATES ShlomoMelmed,M.D.,SeriesEditor Forfurthervolumes: http://www.springer.com/series/5917 OBESITY BEFORE BIRTH Maternal and Prenatal Influences on the Offspring Edited by Robert H. Lustig Professor of Pediatrics University of California San Francisco, CA, USA 123 Editor RobertH.Lustig,MD ProfessorofPediatrics DivisionofEndocrinology Director,WeightAssessmentforTeen andChildHealthProgram UniversityofCalifornia SanFrancisco,CA94143,USA ISSN1566-0729 ISBN978-1-4419-7033-6 e-ISBN978-1-4419-7034-3 DOI10.1007/978-1-4419-7034-3 SpringerNewYorkDordrechtHeidelbergLondon LibraryofCongressControlNumber:2010935733 ©SpringerScience+BusinessMedia,LLC2011 Allrightsreserved.Thisworkmaynotbetranslatedorcopiedinwholeorinpartwithoutthewritten permission of the publisher (Springer Science+Business Media, LLC, 233 Spring Street, New York, NY10013,USA),exceptforbriefexcerptsinconnectionwithreviewsorscholarlyanalysis.Usein connectionwithanyformofinformationstorageandretrieval,electronicadaptation,computersoftware, orbysimilarordissimilarmethodologynowknownorhereafterdevelopedisforbidden. Theuseinthispublicationoftradenames,trademarks,servicemarks,andsimilarterms,eveniftheyare notidentifiedassuch,isnottobetakenasanexpressionofopinionastowhetherornottheyaresubject toproprietaryrights. Whiletheadviceandinformationinthisbookarebelievedtobetrueandaccurateatthedateofgoing to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for anyerrorsoromissionsthatmaybemade.Thepublishermakesnowarranty,expressorimplied,with respecttothematerialcontainedherein. Printedonacid-freepaper SpringerispartofSpringerScience+BusinessMedia(www.springer.com) Theeditorwouldliketodedicatethisvolume tohisfamily:hiswifeJulieandhistwo daughters,MiriamandMeredith.No academiciancouldaskformore understanding,encouragement,sacrifice, andsupport–throughservicecall, out-patient clinic,grantwriting,mentoring others,andabusylectureschedule.Iam blessedbeyondmeasure. Preface Inmybeginningismyend. –T.S.Eliot,#2ofFourQuartets Eliot had no idea that his observations on the life cycle would start even before birth. And indeed, one’s earliest beginning predicts both the timing and means to that end. The concept that obesity was inherent, and not just the sum result of the behaviors of gluttony and sloth was surmised early in the twentieth century, but beganinearnestwiththepostulationofa“thriftygenotype”byJamesNeelin1962. However,thefieldlaydormantforanother30years,awaitingbiologicalandgenetic confirmation. To compound the biological directive, the notion that prenatal bio- logicalinfluencescouldimpactpostnataloutcomesforobesitydatesto1989,when DavidBarker,anepidemiologistfromSouthampton,UK,firstmadetheobservation that now bears his name, the Barker hypothesis. He noted that maternal nutrition impacted on the fetus, such that small for gestational age infants were predicted tobeatincreasedriskforobesityandmetabolicsyndromeinthefuture.Thus,the preceptofdevelopmentalprogrammingtoamendone’sgeneticpredispositionwas advanced. In the interval 21 years since Barker’s discovery, numerous observations have slowlyamendedthesetwocomplementaryhypotheses.Leptin,thefirstgenethatof theenergybalancepathway,wasdiscoveredin1994.Whilealreadydeemedessen- tial for adult body weight regulation, Richard Simerly, then at Oregon Regional Primate Center, showed in animal models in 2004 that leptin likely was molding ourhypothalamievenbeforewetookaswigofbabyformula.Leptinopenedupour understandingoftheenergybalancepathway,includinggenessuchasMC4R,and theirroleinthegeneticsofobesity.Recentgenome-wideassociationscanssuggest that genetic linkages to obesity are primarily in the CNS. We learned in the late 1990sthatlargeforgestationalageandprematureinfantsalsobecameobese;andin theearly2000sthatmaternalobesityandweightgainduringpregnancyarealsorisk factors. Furthermore epigenetics, which led credence to the ability of experiential phenomenainthemothertoaffectgeneticexpressioninthenewborn,wasalreadya hotdisciplinewhenRandyJirtle’sgroupatDukediscoveredin2003thattheycould alteroffspringweightandcolorcoatingeneticallydeterminedAgoutimicethrough vii viii Preface altered maternal nutrition. This line of investigation has expanded exponentially ever since. The phenomenon of epigenetics has tied in very nicely with the above observations, explaining how vertical transmission of obesity can occur exclusive ofDNAbasechanges.Lastly,dataaccruedbyRethaNewboldatNIEHSandBruce BlumbergatUCIrvinein2005foundthatenvironmentaltoxinsnotonlycontribute to obesity in adult animals but also program the liver and adipocyte during gesta- tion.Moreover,eachofthesephenomenahasbeennotedinhumanmodels.Lastly, wenowrecognizethatdevelopmentalprogrammingofobesitycanbepromulgated by actions in numerous target organs in the energy balance pathway. Actions on the hypothalamus can result in an altered energy setpoint; actions on the liver can resultinanalteredmetabolicprofile;andactionsontheadipocytecanresultinan altered storage capacity. These actions are not mutually exclusive, giving rise to phenotypes of hyperphagia (or not), insulin resistance (or not), and subcutaneous vs.visceralfat.Understandingthesetissue-specificeffectsonthesegestationalper- turbationswilllikelyallowforunderstandingofthedifferentobesitysyndromesand theirdownstreamco-morbidities. Takenasawhole,thesevariousphenomenaclearlydemonstratethatdisruption ofthenormalenergybalanceparadigmduringgestationhasprofoundconsequences for the offspring. These observations have led to a new branch of science and medicine:theDevelopmentalOriginsofHealthandDisease(DOHaD).Giventhat (1) the obesity epidemic has gone global; (2) attempts at diet and exercise have failedtocontroltheglobalobesityepidemic;and(3)wenowhaveanepidemicof obese6-month-olds,itistimetothink“outofthebox.”Isthereanexposurethatis causingthis?Arepregnantwomendoingsomethingtomaketheirchildrenfat?Are wepromotingobesitybeforebirth? The purpose of this unique volume is to elucidate, in both animal and human models, the state-of-the-art evidence for each of these phenomena. The evidence, and indeed, our author roster, comes from around the world. Each of the sections of this volume (genetics, epigenetics, developmental programming, environmental obesogens) will start out with the role of pathogenetic mechanism in question in humanobesityandwillthenfollowupwiththeevidenceinanimalmodels.Inthis way,thestrengthandrelevanceofeachofthesepathogeneticmechanismsandtheir effectscanbeassessed. Itishopedthatbyassemblingeachoftheseconceptsinonevolume,wewillbuild aframeworkthatwill(1)informphysicianandpatienteducationintothecausesof the obesity epidemic; (2) provide a nidus for further investigative efforts into the developmentalnatureofobesityandchronicdisease;(3)provideastartingpointfor changesinpoliciestoimprovematernal–childhealth;and(4)providedatatoassist publichealthofficialstomonitorandcontrolenvironmentalexposures,whetherthey benutritionalortoxicological. SanFrancisco,CA RobertH.Lustig March25,2010 Contents 1 Obesity:NatureorNurture? . . . . . . . . . . . . . . . . . . . . . 1 RobertH.Lustig PartI GeneticDisordersLeadingtoObesity 2 TheContributionofHereditytoClinicalObesity . . . . . . . . . 25 JohannaC.AnderssonandAndrewJ.Walley 3 MonogenicDisordersWithintheEnergyBalancePathway . . . . 53 IvyR.Aslan,SayaliA.Ranadive,andChristianVaisse 4 CiliarySyndromesandObesity . . . . . . . . . . . . . . . . . . . 71 DavidS.ParkerandNicholasKatsanis 5 Genome-Wide Association Studies and Human PopulationObesity . . . . . . . . . . . . . . . . . . . . . . . . . . 95 RuthJ.F.LoosandTuomasO.Kilpeläinen PartII EpigeneticChangesandtheDevelopmentofObesity 6 KnownClinicalEpigeneticDisorderswithanObesity Phenotype:Prader–WilliSyndromeandtheGNASLocus . . . . . 115 MerlinG.Butler 7 Evidence for Epigenetic Changes as a Cause ofClinicalObesity . . . . . . . . . . . . . . . . . . . . . . . . . . . 147 GrahamC.BurdgeandKarenA.Lillycrop 8 EpigeneticChangesAssociatedwithIntrauterineGrowth RetardationandAdipogenesis . . . . . . . . . . . . . . . . . . . . 167 SaraE.PinneyandRebeccaA.Simmons PartIII DevelopmentalProgrammingandtheDevelopmentofObesity 9 Exposure to Diabetes In Utero, Offspring Growth, andRiskforObesity . . . . . . . . . . . . . . . . . . . . . . . . . 193 TessaCrumeandDanaDabelea ix x Contents 10 Maternal Weight Gain During Pregnancy andObesityintheOffspring . . . . . . . . . . . . . . . . . . . . . 205 NaomiE.StotlandandJanetC.King 11 IntrauterineGrowthRestriction,SmallforGestational Age,andExperimentalObesity . . . . . . . . . . . . . . . . . . . 215 MichaelG.Ross,IvanHuber,andMinaDesai 12 ExperimentalModelsofMaternalObesityandHigh-Fat DietDuringPregnancyandProgrammedObesity intheOffspring . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 LarissaJanePrior,GeoffreyAlbertHead, andJamesAndrewArmitage 13 High-Carbohydrate IntakeOnlyDuringtheSuckling PeriodResultsinAdult-OnsetObesityinMotheraswell asOffspring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261 MulchandS.PatelandMalathiSrinivasan 14 PrenatalStress,Glucocorticoids,andtheMetabolicSyndrome . . 279 AmandaJ.DrakeandJonathanR.Seckl 15 HypothalamicFetalProgrammingofEnergyHomeostasis . . . . 301 ClementC.CheungandHollyA.Ingraham 16 AdipocyteDevelopmentandExperimentalObesity . . . . . . . . 321 ElviraIsganaitisandMary-ElizabethPatti PartIV EnvironmentalObesogens 17 The Obesogen Hypothesis of Obesity: Overview andHumanEvidence . . . . . . . . . . . . . . . . . . . . . . . . . 355 JerroldJ.Heindel 18 PerinatalExposuretoEndocrineDisruptingChemicals withEstrogenicActivityandtheDevelopmentofObesity . . . . . 367 RethaR.Newbold 19 TheRoleofEnvironmentalObesogensintheObesityEpidemic . 383 AmandaJanesickandBruceBlumberg Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401 Contributors JohannaC.Andersson DepartmentofGenomicsofCommonDisease,Faculty ofMedicine,SchoolofPublicHealth,ImperialCollegeLondon,Hammersmith Hospital,London,UK,[email protected] JamesAndrewArmitage NeuropharmacologyLaboratory,BakerIDIHeartand DiabetesInstitute,Melbourne,VIC,Australia;DepartmentofAnatomyand DevelopmentalBiology,MonashUniversity,Clayton,VIC,Australia, [email protected] IvyR.Aslan DepartmentofEndocrinology,Children’sHospitalandResearch Center,Oakland,74752ndStreet,Oakland,CA93609,USA,[email protected] BruceBlumberg DepartmentofDevelopmentalandCellBiologyand DepartmentofPharmaceuticalSciences,UniversityofCalifornia,Irvine,CA 92697-2300,USA,[email protected] GrahamC.Burdge InstituteofHumanNutrition,UniversityofSouthampton SchoolofMedicine,SouthamptonSO166YD,UK, [email protected] MerlinG.Butler DepartmentsofPsychiatryandBehavioralSciencesand Pediatrics,KansasUniversityMedicalCenter,KansasCity,KS,USA, [email protected] ClementC.Cheung DepartmentsofPediatricsandDepartmentofCellularand MolecularPharmacology,UniversityofCalifornia,SanFrancisco,CA,USA, [email protected] TessaCrume DepartmentofEpidemiology,ColoradoSchoolofPublicHealth, UniversityofColorado,Denver,CO,USA,[email protected] DanaDabelea DepartmentofEpidemiology,ColoradoSchoolofPublicHealth, UniversityofColorado,Denver,CO,USA,[email protected] MinaDesai DepartmentofObstetricsandGynecology,DavidGeffenSchoolof MedicineatHarbor-UCLAMedicalSchool,Torrance,CA,USA, [email protected] xi
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