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葡萄糖对INS-1细胞PTEN和P-AKT表达的影响.docx

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葡萄糖对INS-1细胞PTEN和P-AKT表达的影响 Introduction: Diabetesisachronicmetabolicdisorderthatischaracterizedbyhighbloodglucoselevelsresultingfromdefectsininsulinsecretion,insulinaction,orboth.Insulinisahormoneproducedbythepancreasthatplaysacrucialroleintheregulationofglucosemetabolism.TheInsulin-secretingbeta-cellsofthepancreaticisletsareresponsibleforthesecretionofinsulininresponsetohighbloodglucoselevels.Theinsulinsignalingpathwayregulatesglucosehomeostasis,anditsdysregulationisahallmarkfeatureofdiabetes. Phosphataseandtensinhomolog(PTEN)isatumorsuppressorgenethatisalsoinvolvedintheregulationofglucosehomeostasis.PTENinhibitstheactivityofphosphatidylinositol-3-kinase(PI3K),whichisakeyregulatoroftheinsulinsignalingpathway.PTENdeficiencyleadstoincreasedPI3Kactivity,resultinginhyperactivationoftheinsulinsignalingpathwayandincreasedglucoseuptake.PTENknockoutmiceexhibitincreasedinsulinsensitivityandglucosetolerance.Thus,PTENisanattractivetherapeutictargetfordiabetes. AKT,alsoknownasproteinkinaseB,isadownstreamtargetofPI3Kandplaysacrucialroleintheregulationofglucosemetabolism.AKTisactivatedbyinsulinsignalingandpromotesglucoseuptakebystimulatingtranslocationofglucosetransporter4(GLUT4)totheplasmamembrane.AKTalsoregulatesglucosemetabolismbyinhibitingglycogensynthasekinase3(GSK3),whichinhibitsglycogensynthesis. Glucoseistheprimaryfuelsourceformanycells,includingpancreaticbeta-cells.Glucosestimulatesinsulinsecretionfrombeta-cellsbyincreasingintracellularATPlevels,leadingtotheclosureofATP-sensitivepotassiumchannels(KATP)anddepolarizationoftheplasmamembrane.Thisdepolarizationactivatesvoltage-gatedcalciumchannels(VGCCs),resultinginanincreaseinintracellularcalciumlevelsandinsulinsecretion. Inthisstudy,weinvestigatedtheeffectofglucoseonPTENandP-AKTexpressioninINS-1cells,whichareawell-establishedmodelforstudyingglucose-stimulatedinsulinsecretion. MaterialsandMethods: INS-1cellsweremaintainedinRPMI-1640mediumsupplementedwith10%fetalbovineserumand1%penicillin/streptomycinat37°Cwith5%CO2.Thecells