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生胃酮改善肥胖小鼠肝脏脂质代谢、提高胰岛素敏感性的机制研究.docx

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生胃酮改善肥胖小鼠肝脏脂质代谢、提高胰岛素敏感性的机制研究 Title:Mechanismsunderlyingtheimprovementofhepaticlipidmetabolismandinsulinsensitivityinobesemicebyketogenicdiet Abstract: Theprevalenceofobesityanditsassociatedcomplications,suchasnon-alcoholicfattyliverdisease(NAFLD)andinsulinresistance,hasreachedalarminglevelsworldwide.Recentstudieshaveshownthepotentialofketogenicdietsinamelioratingtheseconditions.Thisresearchaimstoinvestigatethemechanismsunderlyingtheimprovementofhepaticlipidmetabolismandinsulinsensitivityinobesemicebyaketogenicdiet. Introduction: Obesity,characterizedbyexcessiveaccumulationofadiposetissue,isamajorpublichealthconcern,asitincreasestheriskofdevelopingnumerouschronicdiseases,includingNAFLDandinsulinresistance.Theseconditionsarecloselyintertwinedandcontributetothedevelopmentoftype2diabetesandcardiovasculardiseases.Despitethegrowingrecognitionoftheketogenicdietasaneffectivestrategyforweightloss,itspreciseeffectsonhepaticlipidmetabolismandinsulinsensitivityremainpoorlyunderstood. Methods: Inthisstudy,malemicewerefedahigh-fatdiettoinduceobesity.Afterobesitywasestablished,themiceweredividedintotwogroups:thecontrolgroupreceivedastandardchowdiet,andtheexperimentalgroupreceivedaketogenicdietforaspecifiedduration.Bodyweight,liverweight,glucosetolerance,andinsulinsensitivityweremeasured.TheexpressionlevelsofkeyproteinsandgenesinvolvedinhepaticlipidmetabolismandinsulinsignalingpathwayswereassessedusingWesternblotandreal-timepolymerasechainreaction(PCR)analysis. Results: Theketogenicdietresultedinasignificantreductioninbodyweightcomparedtothecontrolgroup.Additionally,liverweightandhepaticlipidcontentwerenotablydecreasedinmicefedtheketogenicdiet.Glucosetolerancewasimproved,asevidencedbyalowerareaunderthecurveinglucosetolerancetests.Insulinsensitivitywasenhanced,asindicatedbythereducedhomeostaticmodelassessmentofinsulinresistance(HOMA-IR)index. Mechanisms: Theimprovementofhepaticlipidmetabolisminmicefedtheketogenicdietcanbeexplainedbyseveralmechanisms.Firstly,theketogenicdietpromoted