Effectsofexercisecombinedwithdietcontrolonglucosemetabolism，developmentofinsulinresistance，andbloodlipidmetabolisminratswithtype2diabetes

Abstract:

Objective：Toinvestigatetheeffectsofexercisecombinedwithdietcontrolonglucosemetabolism，developmentofinsulinresistance，andbloodlipidmetabolisminratswithtype2diabetes.Methods：Atotalof35Wistarratswereincludedinthisstudy.TenWistarratswererandomlyselectedasnormalcontrolgroup，andtheremaining25ratswereusedtoestablishatype2diabetesmodel.Atotalof20modelratswererandomlydividedintomodelcontrolgroupandintervention（exercisecombinedwithdietcontrol）group.Theratsinthenormalcontrolgroupwerefreetomoveandgivenstandardfeed.Theratsinthemodelcontrolgroupwerefreetomoveandgivenhigh-fatandhigh-sugardiet.Swimmingtrainingandstandardfeedweregiventotheratsintheinterventiongroup.Theinterventionperiodinthethreegroupswas8weeks.Bodyweightanddailyfoodintakeoftheratsinthethreegroupsweremeasuredbeforeexperiment，aftermodelingandbeforeintervention，andafter4and8weeksofintervention.Beforeinterventionandafter8weeksofintervention，thelevelsoffastingbloodglucose（FBG），fastinginsulin（FINS），triglyceride（TG），cholesterol（TC），andlow-densitylipoproteincholesterol（LDL-C）weremeasured，andglucosetolerancetest（GTT）andinsulintolerancetest（ITT）wereperformedtoassessinsulinresistance.Afterexercise，thepancreatictissuewastakentodeterminetheactivitiesofglucoseki－nase（GK）andadenosinetriphosphatase（ATPase）；themRNAexpressionofinsulinreceptorsubstrate-1（IRS-1），phosphoinositide3-kinase（PI3K），proteinkinaseB（PKB），andmammaliantargetofrapamycin（mTOR）inthepancreatictissuewasdeterminedbyreal-timepolymerasechainreaction；theproteinexpressionofIRS-1，phosphorylatedIRS-1（p-IRS-1），PI3K，PKB，phosphorylatedPKB（p-PKB），mTOR，andphosphorylatedmTOR（p-mTOR）inthepancreatictissuewasdeterminedbyWesternblot.Results：①After4and8weeksofintervention，theinterventiongrouphadasignificantlyhigherbodyweightthanthemodelcontrolgroup（P<0.05），andtherewasasignificantdifferenceindailyfoodintakebetweenthetwogroups（P<0.05）.②After8weeksofintervention，theinterventiongrouphadsignificantlylowerlevelsofFBGandFINS，homeostasismodelassessmentofinsulinresistance，areaunderthereceiveroperatingcharacteristiccurve（AUC）GTT，andAUCITTthanthemodelcontrolgroup（P<0.05）.③After8weeksofinterven－tion，theinterventiongrouphadsignificantlylowerlevelsofTG，TC，andLDL-Cthanthemodelcontrolgroup（P<0.05）.④After8weeksofintervention，theinterventiongrouphadsignificantlyhigherGKandATPaseactivitiesinthepancreatictissuecomparedwiththemodelcontrolgroup（P<0.05）.⑤After8weeksofintervention，theinterventiongrouphadsignificantlyhighermRNAexpressionofIRS-1，PI3K，andPKBinthepancreatictissueandsignificantlylowermRNAexpressionofmTORinthepancreatictissuecomparedwiththemodelcontrolgroup（P<0.05）.⑥After8weeksofintervention，theinterventiongrouphadsignificantlyhigherproteinexpressionofIRS-1，p-IRS-1，PI3K，PKB，andp-PKBinthepancreatictissueandsignificantlylowerproteinexpressionofmTORandp-mTORcomparedwiththemodelcontrolgroup（P<0.05）.Conclusion：Exercisecombinedwithdietcontrolcancontrolthebloodglucoselevelofratswithtype2diabetes，alleviateinsulinresistanceanddyslipidemia，increasetheactivitiesofGKandATPaseinthepancreatictissue，andregulatetheIRS/PI3K-Aktsignalingpathway.