Oleanolic Acid Reduces Hyperglycemia beyond Treatment Period with AktFoxO1-Induced Suppression of Hepatic Gluconeogenesis in Type-2 Diabetic Mice 英文参考文献.docVIP

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Oleanolic Acid Reduces Hyperglycemia beyond Treatment Period with AktFoxO1-Induced Suppression of Hepatic Gluconeogenesis in Type-2 Diabetic Mice 英文参考文献.doc

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Oleanolic Acid Reduces Hyperglycemia beyond Treatment Period with AktFoxO1-Induced Suppression of Hepatic Gluconeogenesis in Type-2 Diabetic Mice 英文参考文献

OleanolicAcidReducesHyperglycemiabeyond TreatmentPeriodwithAkt/FoxO1-InducedSuppression ofHepaticGluconeogenesisinType-2DiabeticMice Xiao-YiZeng1,Yi-PingWang1,JamesCantley2,TristanJ.Iseli2,JuanCarlosMolero1, BronwynD.Hegarty2,EdwardW.Kraegen2,YangYe3,Ji-MingYe1,2,3* 1MolecularPharmacologyforDiabetes,HealthInnovationsResearchInstituteandSchoolofHealthSciences,RMITUniversity,Melbourne,Victoria,Australia,2Diabetes andObesityProgram,GarvanInstituteofMedicalResearch,Sydney,NewSouthWales,Australia,3ShanghaiInstituteofMateriaMedica,ChineseAcademyofSciences, Shanghai,China Abstract Thepresentstudyinvestigatedthechronicefficacyofoleanolicacid(OA),atriterpenoidselectedfromourrecentscreening, onhyperglycemiaintype-2diabeticmice.C57BL/6Jmicewerefedahigh-fatdietfollowedbylowdosesofstreptozotocin togenerateatype-2diabeticmodel.OA(100mg/kg/day)wasadministeredorallyfor2weekswithitseffectsmonitoredfor 6 weeks. High-fat feeding and streptozotocin generated a steady hyperglycemia (21.261.1mM) but OA administration reversedthehyperglycemiaby,60%.Interestingly,afterthecessationofOAadministration,thereversedhyperglycemia was sustained for the entire post-treatment period of the study (4 weeks) despite the reoccurrence of dyslipidemia. Examinationofinsulinsecretionandpancreasmorphologydidnotindicateimprovedb-cellfunctionasalikelymechanism. Urine glucose loss was decreased with substantial improvement of diabetic nephropathy after the OA treatment. Pair- feedingtheOA-treatedmicetoanuntreatedgroupruledoutfoodintakeasamainfactorattributableforthissustained reduction in hyperglycemia. Studies with the use of glucose tracers revealed no increase in glucose influx into muscle, adiposetissueorliverintheOA-treatedmice.Finally,weanalyzedkeyregulatorsofgluconeogenesisintheliverandfound significantincreasesinthephosphorylationofbothAktandFoxO1aftertreatmentwithOA.Importantly,theseincreases were significantly correlated with a down-regulation of glucose-6-phosphatase expression. Our findings sugge