2023
Estradiol cycling drives female obesogenic adipocyte hyperplasia
del M. Saavedra-Peña R, Taylor N, Flannery C, Rodeheffer M. Estradiol cycling drives female obesogenic adipocyte hyperplasia. Cell Reports 2023, 42: 112390. PMID: 37053070, PMCID: PMC10567995, DOI: 10.1016/j.celrep.2023.112390.Peer-Reviewed Original ResearchConceptsAdipocyte precursor cellsHigh-fat dietAdipocyte hyperplasiaHFD feedingVisceral WATDifferential fat distributionAdipose tissue distributionEstrogen receptor αWAT distributionFat distributionOvariectomized femalesHyperplasiaMice showEstrous cycleReceptor αTissue distributionPrecursor cellsObesityAPC proliferationTissue microenvironmentProliferationFemalesSexOnsetFeeding
2014
The H19/let-7 double-negative feedback loop contributes to glucose metabolism in muscle cells
Gao Y, Wu F, Zhou J, Yan L, Jurczak MJ, Lee HY, Yang L, Mueller M, Zhou XB, Dandolo L, Szendroedi J, Roden M, Flannery C, Taylor H, Carmichael GG, Shulman GI, Huang Y. The H19/let-7 double-negative feedback loop contributes to glucose metabolism in muscle cells. Nucleic Acids Research 2014, 42: 13799-13811. PMID: 25399420, PMCID: PMC4267628, DOI: 10.1093/nar/gku1160.Peer-Reviewed Original ResearchConceptsDouble-negative feedback loopLet-7PI3K/Akt-dependent phosphorylationLet-7 targetsHuman genetic disordersAkt-dependent phosphorylationMuscle cellsInsulin-resistant rodentsSponge lncRNAsMolecular spongeH19 lncRNAFeedback loopGrowth controlDepletion resultsH19Impaired insulinLncRNAsTarget miRNAGlucose uptakeGenetic disordersBiogenesisCellsKSRPPhosphorylationMicroRNAs
2012
Skeletal Muscle Insulin Resistance Promotes Increased Hepatic De Novo Lipogenesis, Hyperlipidemia, and Hepatic Steatosis in the Elderly
Flannery C, Dufour S, Rabøl R, Shulman GI, Petersen KF. Skeletal Muscle Insulin Resistance Promotes Increased Hepatic De Novo Lipogenesis, Hyperlipidemia, and Hepatic Steatosis in the Elderly. Diabetes 2012, 61: 2711-2717. PMID: 22829450, PMCID: PMC3478531, DOI: 10.2337/db12-0206.Peer-Reviewed Original ResearchConceptsHepatic de novo lipogenesisNonalcoholic fatty liver diseaseDe novo lipogenesisMuscle insulin resistanceInsulin resistanceElderly subjectsNovo lipogenesisYoung subjectsInsulin resistance promotesSedentary elderly subjectsFatty liver diseaseHigh-carbohydrate mealHepatic triglyceride contentType 2 diabetesMuscle glycogen synthesisGlycogen synthesisLiver glycogen synthesisLiver diseaseNormal weightHepatic steatosisPostprandial changesPlasma TGLiver glycogenHyperlipidemiaMuscle glycogen
2010
Knockdown of the gene encoding Drosophila tribbles homologue 3 (Trib3) improves insulin sensitivity through peroxisome proliferator-activated receptor-γ (PPAR-γ) activation in a rat model of insulin resistance
Weismann D, Erion DM, Ignatova-Todorava I, Nagai Y, Stark R, Hsiao JJ, Flannery C, Birkenfeld AL, May T, Kahn M, Zhang D, Yu XX, Murray SF, Bhanot S, Monia BP, Cline GW, Shulman GI, Samuel VT. Knockdown of the gene encoding Drosophila tribbles homologue 3 (Trib3) improves insulin sensitivity through peroxisome proliferator-activated receptor-γ (PPAR-γ) activation in a rat model of insulin resistance. Diabetologia 2010, 54: 935-944. PMID: 21190014, PMCID: PMC4061906, DOI: 10.1007/s00125-010-1984-5.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzhydryl CompoundsDiabetes Mellitus, Type 2Disease Models, AnimalEpoxy CompoundsGlucose Clamp TechniqueImmunoblottingInsulin ResistanceMaleOligonucleotides, AntisensePPAR gammaProtein KinasesProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionConceptsTribbles homologue 3Euglycaemic hyperinsulinaemic clampWhite adipose tissueInsulin sensitivityAdipose tissueAntisense oligonucleotideInsulin-stimulated whole-body glucose uptakeWhole-body glucose uptakeConclusions/interpretationThese dataTissue-specific insulin sensitivityGlucose uptakeSkeletal muscle glucose uptakeWhite adipose tissue massPlasma HDL cholesterolRole of PPARAdipose tissue massMuscle glucose uptakeEndogenous glucose productionExpression of PPARInsulin-sensitising effectsDependent mannerViral proto-oncogeneHDL cholesterolAkt2 activityInsulin resistance
2009
Prevention of Hepatic Steatosis and Hepatic Insulin Resistance by Knockdown of cAMP Response Element-Binding Protein
Erion DM, Ignatova ID, Yonemitsu S, Nagai Y, Chatterjee P, Weismann D, Hsiao JJ, Zhang D, Iwasaki T, Stark R, Flannery C, Kahn M, Carmean CM, Yu XX, Murray SF, Bhanot S, Monia BP, Cline GW, Samuel VT, Shulman GI. Prevention of Hepatic Steatosis and Hepatic Insulin Resistance by Knockdown of cAMP Response Element-Binding Protein. Cell Metabolism 2009, 10: 499-506. PMID: 19945407, PMCID: PMC2799933, DOI: 10.1016/j.cmet.2009.10.007.Peer-Reviewed Original ResearchConceptsHepatic insulin resistanceNonalcoholic fatty liver diseaseCAMP response element-binding proteinInsulin resistanceResponse element-binding proteinASO treatmentElement-binding proteinCREB expressionType 2 diabetes mellitusOb/ob miceFatty liver diseaseHepatic triglyceride contentPlasma glucose concentrationFed rat modelAttractive therapeutic targetAntisense oligonucleotideDiabetes mellitusLiver diseaseZDF ratsHepatic steatosisOb micePostprandial hyperglycemiaPlasma cholesterolRat modelTriglyceride concentrations