2012
5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model
Xu L, Kim JK, Bai Q, Zhang X, Kakiyama G, Min HK, Sanyal AJ, Pandak WM, Ren S. 5-Cholesten-3β,25-Diol 3-Sulfate Decreases Lipid Accumulation in Diet-Induced Nonalcoholic Fatty Liver Disease Mouse Model. Molecular Pharmacology 2012, 83: 648-658. PMID: 23258548, PMCID: PMC3583496, DOI: 10.1124/mol.112.081505.Peer-Reviewed Original ResearchMeSH KeywordsAcetyl-CoA CarboxylaseAcetyltransferasesAnimalsCholesterol EstersDiet, High-FatFas ReceptorFatty AcidsFatty LiverFemaleGene ExpressionGlucose Tolerance TestGlycerol-3-Phosphate O-AcyltransferaseHydroxycholesterolsInflammationInsulinInsulin ResistanceInterleukin-1alphaInterleukin-1betaLipid MetabolismLipidsLiverMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal TransductionSterol Regulatory Element Binding Protein 1Tumor Necrosis Factor-alphaConceptsNonalcoholic fatty liver diseaseHigh-fat dietLong-term treatmentAcute treatmentTolerance testLipid accumulationMouse modelDiet-induced NAFLD mouse modelNonalcoholic fatty liver disease (NAFLD) mouse modelSREBP-1cLipid homeostasisFatty liver diseaseLiver X receptor αNAFLD mouse modelGlucose tolerance testSerum lipid levelsInsulin tolerance testHepatic lipid accumulationDisease mouse modelDecreases lipid accumulationTumor necrosis factorLipid-induced inflammationAcetyl-CoA carboxylase 1X receptor αSREBP-1c expressionCholesterol metabolite, 5-cholesten-3β-25-diol-3-sulfate, promotes hepatic proliferation in mice
Zhang X, Bai Q, Kakiyama G, Xu L, Kim JK, Pandak WM, Ren S. Cholesterol metabolite, 5-cholesten-3β-25-diol-3-sulfate, promotes hepatic proliferation in mice. The Journal Of Steroid Biochemistry And Molecular Biology 2012, 132: 262-270. PMID: 22732306, PMCID: PMC3463675, DOI: 10.1016/j.jsbmb.2012.06.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell CycleCell ProliferationCholesterolCholesterol EstersDNA ReplicationGene Expression RegulationHydrocarbons, FluorinatedHydroxycholesterolsLiverLiver X ReceptorsMiceMice, Inbred C57BLOrphan Nuclear ReceptorsSignal TransductionSulfonamidesSulfotransferasesTissue DistributionUp-RegulationConceptsLiver X receptorHepatic proliferationSynthetic LXR agonist T0901317LXR agonist T0901317PCNA labeling indexDose-dependent mannerSuppresses cell proliferationOxysterol sulfationOxysterol sulfotransferaseProliferation gene expressionAgonist T0901317Cholesterol metabolitesLabeling indexEndogenous ligandLiver proliferationX receptorHepatic DNA replicationHepatocyte proliferationSREBP-1cNovel regulatory pathwayPCR arrayCell proliferationAdministrationPotent regulatorOxysterols
2010
Sulfation of 25-hydroxycholesterol by SULT2B1b decreases cellular lipids via the LXR/SREBP-1c signaling pathway in human aortic endothelial cells
Bai Q, Xu L, Kakiyama G, Runge-Morris MA, Hylemon PB, Yin L, Pandak WM, Ren S. Sulfation of 25-hydroxycholesterol by SULT2B1b decreases cellular lipids via the LXR/SREBP-1c signaling pathway in human aortic endothelial cells. Atherosclerosis 2010, 214: 350-356. PMID: 21146170, PMCID: PMC3031658, DOI: 10.1016/j.atherosclerosis.2010.11.021.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedCholesterol EstersChromatography, High Pressure LiquidEndothelial CellsFatty Acids, NonesterifiedGene Expression RegulationHumansHydrocarbons, FluorinatedHydroxycholesterolsLiver X ReceptorsOrphan Nuclear ReceptorsRNA, MessengerSignal TransductionSterol Regulatory Element Binding Protein 1SulfonamidesSulfotransferasesTime FactorsTransfectionTriglyceridesConceptsHuman aortic endothelial cellsLipid metabolismAortic endothelial cellsSULT2B1b overexpressionSREBP-1cEndothelial cellsIntracellular lipid homeostasisOxysterol sulfotransferaseReceptor agonistLipid levelsPresence of T0901317Cellular lipid levelsLipid homeostasisRecombinant adenovirusACC-1Protein levelsSULT2B1bSulfated metabolitesMetabolismCellular lipidsOverexpressionKey regulatorSimilar resultsCells