Jianying Dong
Associate Research Scientist (Endocrinology)Cards
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Endocrinology
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Associate Research Scientist (Endocrinology)
Appointments
Endocrinology
Associate Research ScientistPrimary
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Jianying Dong's published research.
Publications Timeline
A big-picture view of Jianying Dong's research output by year.
Gerald I Shulman, MD, PhD, MACP, MACE, FRCP
Lawrence Young, MD
Tamas Horvath, DVM, PhD
13Publications
1,981Citations
Publications
2020
Leptin mediates postprandial increases in body temperature through hypothalamus–adrenal medulla–adipose tissue crosstalk
Perry RJ, Lyu K, Rabin-Court A, Dong J, Li X, Yang Y, Qing H, Wang A, Yang X, Shulman GI. Leptin mediates postprandial increases in body temperature through hypothalamus–adrenal medulla–adipose tissue crosstalk. Journal Of Clinical Investigation 2020, 130: 2001-2016. PMID: 32149734, PMCID: PMC7108915, DOI: 10.1172/jci134699.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsBrown adipose tissueLeptin concentrationsBody temperatureAdrenomedullary catecholamine secretionPlasma leptin concentrationsAdipose tissue lipolysisFasting-induced reductionFeeding-induced increaseMeal ingestionPlasma catecholaminesPostprandial increaseCatecholamine secretionObese ratsTissue lipolysisLean ratsAdrenergic activationAdipose tissueTissue crosstalkWeight gainIntragastric infusionRatsLeptinBolusLipolysisFatty acids
2014
A Role for Mitochondrial Phosphoenolpyruvate Carboxykinase (PEPCK-M) in the Regulation of Hepatic Gluconeogenesis*
Stark R, Guebre-Egziabher F, Zhao X, Feriod C, Dong J, Alves TC, Ioja S, Pongratz RL, Bhanot S, Roden M, Cline GW, Shulman GI, Kibbey RG. A Role for Mitochondrial Phosphoenolpyruvate Carboxykinase (PEPCK-M) in the Regulation of Hepatic Gluconeogenesis*. Journal Of Biological Chemistry 2014, 289: 7257-7263. PMID: 24497630, PMCID: PMC3953244, DOI: 10.1074/jbc.c113.544759.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimal FeedAnimalsBlood GlucoseFood DeprivationGene Expression Regulation, EnzymologicGene SilencingGluconeogenesisGlycerolGlycogenGuanosine TriphosphateHepatocytesHomeostasisInsulinIntracellular Signaling Peptides and ProteinsIsoenzymesLactic AcidLiverMaleMitochondriaOligonucleotides, AntisenseOxygenOxygen ConsumptionPhosphoenolpyruvate Carboxykinase (GTP)RatsRats, Sprague-Dawley
2010
Resistance to High-fat Diet-Induced Obesity and Insulin Resistance in Mice with Very Long-Chain Acyl-CoA Dehydrogenase Deficiency
Zhang D, Christianson J, Liu Z, Tian L, Choi C, Neschen S, Dong J, Wood P, Shulman G. Resistance to High-fat Diet-Induced Obesity and Insulin Resistance in Mice with Very Long-Chain Acyl-CoA Dehydrogenase Deficiency. Cell Metabolism 2010, 12: 103. DOI: 10.1016/j.cmet.2010.06.004.Peer-Reviewed Original ResearchResistance to High-Fat Diet-Induced Obesity and Insulin Resistance in Mice with Very Long-Chain Acyl-CoA Dehydrogenase Deficiency
Zhang D, Christianson J, Liu ZX, Tian L, Choi CS, Neschen S, Dong J, Wood PA, Shulman GI. Resistance to High-Fat Diet-Induced Obesity and Insulin Resistance in Mice with Very Long-Chain Acyl-CoA Dehydrogenase Deficiency. Cell Metabolism 2010, 11: 402-411. PMID: 20444420, PMCID: PMC3146169, DOI: 10.1016/j.cmet.2010.03.012.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsMitochondrial fatty acid oxidationFatty acid oxidationMitochondrial fatty acid oxidation enzymesProtein kinase CthetaLong-chain acyl-CoA dehydrogenaseAcid oxidationFatty acid oxidation enzymesAcyl-CoA dehydrogenaseDiet-induced obesityMuscle insulin resistanceLong-Chain AcylInsulin resistanceCellular metabolismOxidation enzymesDiacylglycerol contentHigh-fat diet-induced obesityFat Diet-Induced ObesityType 2 diabetesImportant energy sourceCoA dehydrogenase deficiencyChronic activationInsulin sensitivity
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 ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFood 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
2007
Mitochondrial dysfunction due to long-chain Acyl-CoA dehydrogenase deficiency causes hepatic steatosis and hepatic insulin resistance
Zhang D, Liu ZX, Choi CS, Tian L, Kibbey R, Dong J, Cline GW, Wood PA, Shulman GI. Mitochondrial dysfunction due to long-chain Acyl-CoA dehydrogenase deficiency causes hepatic steatosis and hepatic insulin resistance. Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 17075-17080. PMID: 17940018, PMCID: PMC2040460, DOI: 10.1073/pnas.0707060104.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAcyl Coenzyme AAcyl-CoA Dehydrogenase, Long-ChainAnimalsCalorimetryCarbon IsotopesDiglyceridesEnergy MetabolismFatty LiverGene Expression RegulationGlucoseHomeostasisInsulinInsulin ResistanceLiverMiceMitochondriaMuscle, SkeletalOxidation-ReductionProtein Kinase C-epsilonSignal TransductionTriglyceridesConceptsLong-chain acyl-CoA dehydrogenaseHepatic insulin resistanceInsulin stimulationMitochondrial functionInsulin resistanceMitochondrial fatty acid oxidation capacityMitochondrial fatty acid oxidationAcyl-CoA dehydrogenaseHepatic steatosisFatty acid oxidation capacityAkt2 activationDe novo synthesisFatty acid oxidationPKCepsilon activationKey enzymeHyperinsulinemic-euglycemic clampLong-chain acyl-CoA dehydrogenase deficiencyType 2 diabetesPrimary defectMitochondrial dysfunctionHepatic glucose productionAcyl-CoA dehydrogenase deficiencyPKCepsilon activityNovo synthesisDiacylglycerol accumulationAging-Associated Reductions in AMP-Activated Protein Kinase Activity and Mitochondrial Biogenesis
Reznick RM, Zong H, Li J, Morino K, Moore IK, Yu HJ, Liu ZX, Dong J, Mustard KJ, Hawley SA, Befroy D, Pypaert M, Hardie DG, Young LH, Shulman GI. Aging-Associated Reductions in AMP-Activated Protein Kinase Activity and Mitochondrial Biogenesis. Cell Metabolism 2007, 5: 151-156. PMID: 17276357, PMCID: PMC1885964, DOI: 10.1016/j.cmet.2007.01.008.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsIntracellular lipid metabolismMitochondrial biogenesisAMPK activityMitochondrial functionProtein kinase activityLipid metabolismProtein kinaseKinase activityAge-associated reductionBiogenesisOld ratsAMPKSkeletal muscleRecent studiesInsulin resistanceChronic activationMetabolismAcute stimulationFat oxidationImportant roleAcid feedingKinaseRatsActivityRegulationn-3 Fatty Acids Preserve Insulin Sensitivity In Vivo in a Peroxisome Proliferator–Activated Receptor-α–Dependent Manner
Neschen S, Morino K, Dong J, Wang-Fischer Y, Cline GW, Romanelli AJ, Rossbacher J, Moore IK, Regittnig W, Munoz DS, Kim JH, Shulman GI. n-3 Fatty Acids Preserve Insulin Sensitivity In Vivo in a Peroxisome Proliferator–Activated Receptor-α–Dependent Manner. Diabetes 2007, 56: 1034-1041. PMID: 17251275, DOI: 10.2337/db06-1206.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsPPAR alpha-null miceHepatic insulin resistanceHigh-fat diet-induced hepatic insulin resistanceDiacylglycerol-dependent mannerInsulin resistanceWild-type miceFish oil dietOil dietPEPCK gene expressionNull miceDiet-induced hepatic insulin resistanceInsulin sensitivityPPAR-alpha nullSafflower oilFatty acidsGene expressionIsocaloric high-fat dietHigh-fat diet-induced insulin resistanceDiet-induced insulin resistancePeroxisome proliferator-activated receptorLipid abundanceFish oil replacementFish oilHigh-fat dietInsulin-mediated suppression
2005
Adipocyte-Specific Overexpression of FOXC2 Prevents Diet-Induced Increases in Intramuscular Fatty Acyl CoA and Insulin Resistance
Kim JK, Kim HJ, Park SY, Cederberg A, Westergren R, Nilsson D, Higashimori T, Cho YR, Liu ZX, Dong J, Cline GW, Enerback S, Shulman GI. Adipocyte-Specific Overexpression of FOXC2 Prevents Diet-Induced Increases in Intramuscular Fatty Acyl CoA and Insulin Resistance. Diabetes 2005, 54: 1657-1663. PMID: 15919786, DOI: 10.2337/diabetes.54.6.1657.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsWild-type miceInsulin resistanceType 2 diabetesAdipocyte-specific overexpressionHigh-fat feedingTg miceGlucose metabolismTransgenic miceDiet-induced hepatic insulin resistanceChronic high-fat feedingTissue-specific insulin actionWhole-body fat massWhole-body glucose metabolismDiet-induced insulin resistanceIntracellular fat contentDiet-induced obesityHigh-fat dietInsulin-mediated suppressionFatty acyl-CoA levelsHepatic insulin resistanceNovel therapeutic targetHepatic glucose productionAcyl-CoA levelsIntramuscular accumulationGlucose intolerance