2009
The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator-1 β in the Pathogenesis of Fructose-Induced Insulin Resistance
Nagai Y, Yonemitsu S, Erion DM, Iwasaki T, Stark R, Weismann D, Dong J, Zhang D, Jurczak MJ, Löffler MG, Cresswell J, Yu XX, Murray SF, Bhanot S, Monia BP, Bogan JS, Samuel V, Shulman GI. The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator-1 β in the Pathogenesis of Fructose-Induced Insulin Resistance. Cell Metabolism 2009, 9: 252-264. PMID: 19254570, PMCID: PMC3131094, DOI: 10.1016/j.cmet.2009.01.011.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsDietFructoseGene ExpressionHepatocytesHumansInsulin ResistanceLiverMaleMiceOligonucleotides, AntisensePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsRats, Sprague-DawleyRNA-Binding ProteinsSterol Regulatory Element Binding Protein 1Transcription FactorsConceptsInsulin resistancePeroxisome proliferator-activated receptor gamma coactivator 1 betaInsulin-stimulated whole-body glucose disposalWhole-body glucose disposalPGC-1betaTreatment of NAFLDFructose-Induced Insulin ResistanceHepatic insulin resistanceWhite adipose tissueDe novo lipogenesisSREBP-1Downstream lipogenic genesReceptor γ coactivatorGlucose disposalInsulin-stimulated statesHepatic lipogenesisNovo lipogenesisTherapeutic targetAdipose tissuePeroxisome proliferatorLipogenic genesΓ coactivatorGlucose uptakePathogenesisMetabolic phenotype
2008
N-acylphosphatidylethanolamine, a Gut- Derived Circulating Factor Induced by Fat Ingestion, Inhibits Food Intake
Gillum MP, Zhang D, Zhang XM, Erion DM, Jamison RA, Choi C, Dong J, Shanabrough M, Duenas HR, Frederick DW, Hsiao JJ, Horvath TL, Lo CM, Tso P, Cline GW, Shulman GI. N-acylphosphatidylethanolamine, a Gut- Derived Circulating Factor Induced by Fat Ingestion, Inhibits Food Intake. Cell 2008, 135: 813-824. PMID: 19041747, PMCID: PMC2643061, DOI: 10.1016/j.cell.2008.10.043.Peer-Reviewed Original ResearchConceptsFood intakeInhibits food intakeTreatment of obesityNovel therapeutic targetCentral nervous systemUnknown physiological significanceFat ingestionCirculating factorsN-acylphosphatidylethanolaminePlasma lipidsIntracerebroventricular infusionPhysiologic dosesSystemic administrationTherapeutic targetBody weightNervous systemIngested fatSmall intestineIntakeTaste aversionInfusionPhysiological significanceNanomolar amountsObesityHypothalamus
2004
Inactivation of fatty acid transport protein 1 prevents fat-induced insulin resistance in skeletal muscle
Kim JK, Gimeno RE, Higashimori T, Kim HJ, Choi H, Punreddy S, Mozell RL, Tan G, Stricker-Krongrad A, Hirsch DJ, Fillmore JJ, Liu ZX, Dong J, Cline G, Stahl A, Lodish HF, Shulman GI. Inactivation of fatty acid transport protein 1 prevents fat-induced insulin resistance in skeletal muscle. Journal Of Clinical Investigation 2004, 113: 756-763. PMID: 14991074, PMCID: PMC351314, DOI: 10.1172/jci18917.Peer-Reviewed Original ResearchMeSH KeywordsAdiponectinAdipose TissueAnimalsBlood GlucoseCarrier ProteinsDiabetes Mellitus, Type 2Fatty Acid Transport ProteinsFatty AcidsFemaleGene DeletionGene Expression RegulationGlucoseInsulinInsulin ResistanceIntercellular Signaling Peptides and ProteinsMaleMembrane Transport ProteinsMiceMice, KnockoutModels, GeneticMuscle, SkeletalPatch-Clamp TechniquesPhenotypeProteinsSignal TransductionConceptsFatty acid transport protein 1Fatty acid metabolitesInsulin resistanceType 2 diabetesWhole-body adiposityKO miceAcid metabolitesSkeletal muscleChronic high-fat feedingAcute lipid infusionRegular chow dietHigh-fat feedingNovel therapeutic targetFatty acid uptakeIntramuscular accumulationLipid infusionChow dietInsulin sensitivityGlucose homeostasisTherapeutic targetInsulin actionAcid uptakeProtein 1Tissue expressionMice