2012
Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review
Behl M, Rao D, Aagaard K, Davidson T, Levin E, Slotkin T, Srinivasan S, Wallinga D, White M, Walker V, Thayer K, Holloway A. Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review. Environmental Health Perspectives 2012, 121: 170-180. PMID: 23232494, PMCID: PMC3569686, DOI: 10.1289/ehp.1205404.Peer-Reviewed Original ResearchConceptsMaternal smokingChildhood obesityMetabolic disordersRisk factorsChildhood overweight/obesityUnmeasured residual confoundingOverweight/obesityRisk of obesityCurrent epidemiological dataType 2 diabetesPotential risk factorsType 1 diabetesEarly life exposureEnvironmental chemicalsExperimental animal studiesPerinatal exposureMetabolic syndromeNicotine exposureMetabolic outcomesResidual confoundingEpidemiological dataCigarette smokeObesitySmokingAnimal studies
2004
IRS‐2 mediates the antiapoptotic effect of insulin in neonatal hepatocytes
Valverde A, Fabregat I, Burks D, White M, Benito M. IRS‐2 mediates the antiapoptotic effect of insulin in neonatal hepatocytes. Hepatology 2004, 40: 1285-1294. PMID: 15565601, DOI: 10.1002/hep.20485.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Bcl-X ProteinBlood ProteinsCarrier ProteinsEpidermal Growth FactorFemaleForkhead Box Protein O1Forkhead Transcription FactorsGene ExpressionHepatocytesHypoglycemic AgentsInsulinInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiceMice, Mutant StrainsPhosphatidylinositol 3-KinasesPhosphoproteinsPregnancyProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Signal TransductionTranscription FactorsConceptsCaspase-3 activityIRS-2Caspase-3 activationGene expressionWild-type hepatocytesDominant negative FoxO1Wild-type cellsSerum withdrawal-induced apoptosisInsulin receptor substrateWithdrawal-induced apoptosisAnti-apoptotic gene expressionImmortalized hepatocyte cell linesIRS-2 signalingPIP3 generationProapoptotic gene expressionAntiapoptotic gene expressionProlonged insulin treatmentEpidermal growth factorActive FoxO1Receptor substrateNeonatal hepatocytesProapoptotic genesAntiapoptotic genesCaspase-8Serum withdrawal
2003
Molecular Mechanisms of Insulin Resistance in IRS-2-Deficient Hepatocytes
Valverde A, Burks D, Fabregat I, Fisher T, Carretero J, White M, Benito M. Molecular Mechanisms of Insulin Resistance in IRS-2-Deficient Hepatocytes. Diabetes 2003, 52: 2239-2248. PMID: 12941762, DOI: 10.2337/diabetes.52.9.2239.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsAnimals, NewbornAntigens, Polyomavirus TransformingCell Line, TransformedFemaleForkhead Box Protein O1Forkhead Transcription FactorsGluconeogenesisGlucose-6-PhosphataseGlycogen SynthaseGlycogen Synthase Kinase 3HepatocytesHypoglycemic AgentsInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceIntracellular Signaling Peptides and ProteinsIsoenzymesMaleMiceMice, Mutant StrainsPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoenolpyruvate Carboxykinase (GTP)PhosphoproteinsPregnancyProtein Kinase CProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRetroviridaeSignal TransductionTranscription FactorsConceptsGluconeogenic gene expressionIRS-2Gene expressionPrimary hepatocytesAtypical protein kinase CIRS-1-associated phosphatidylinositolIRS-1 tyrosine phosphorylationInsulin-induced phosphatidylinositolTranslocation of phosphatidylinositolInsulin receptor substrateGlycogen synthase kinaseProtein kinase CActivation of AktDownstream phosphatidylinositolTyrosine phosphorylationPlasma membraneReceptor substrateGlycogen synthase activityMolecular mechanismsSynthase kinaseInsulin stimulationKinase CHepatocyte cell linePhosphatidylinositolFunctional insulin
1999
Exclusion of insulin receptor substrate 2 (IRS-2) as a major locus for early-onset autosomal dominant type 2 diabetes.
Bektas A, Warram J, White M, Krolewski A, Doria A. Exclusion of insulin receptor substrate 2 (IRS-2) as a major locus for early-onset autosomal dominant type 2 diabetes. Diabetes 1999, 48: 640-642. PMID: 10078569, DOI: 10.2337/diabetes.48.3.640.Peer-Reviewed Original ResearchAdultAge of OnsetChromosome MappingChromosomes, Human, Pair 13Diabetes Mellitus, Type 2Diabetes, GestationalFemaleGenes, DominantGenetic LinkageGenetic MarkersGlucose IntoleranceHumansInsulin Receptor Substrate ProteinsIntracellular Signaling Peptides and ProteinsLod ScoreMalePhosphoproteinsPregnancyReceptor, InsulinReference Values