Effects Of Piperine On Key Targets Of AMPK Pathway In Insulin Resistance Model Of3T3-L1Adipocytes

Objective:Effects of PIP on glucose metabolism disorder and AMPKα, LEP, APN, GLUT4of AMPK pathway in insulin resistance model of3T3-L1adipocytes induced bydexamethasone were investigated, in order to explore possible mechanism of PIP inimproving glucose metabolism.Methods:13T3-L1preadipocytes were induced to differentiate into adipocytes by IBMX,dexamethasone and insulin mixture, then identify its successful differentiation.Adipocyte insulin resistance model was established by1μM dexamethasone, and weobserved the regulation of PIP on glucose metabolism disorder.2The contents of APN, LEP in supernatant were detected by ELISA method;RT-PCR was used to detect expression of AMPKα, APN, LEP and GLUT4mRNA;Western blot was used to detect levels of AMPKα, p-AMPKα and GLUT4proteinexpression.Results:1Glucose consumption of IR model group were significantly lower than controlgroup with1μM dexamethasone for48h(P <0.001),which showed IR Adipocytesmodel was successfully established;compared with control group,PIP couldsignificantly increase glucose consumption of IR model (P<0.01,P<0.001), and theglucose consumption was significantly increased with PIP of10μM for only12hours.2Compared with IR model group, PIP could significantly increase the contents ofAPN of supernatant (P<0.05,P<0.01,P<0.001); PIP could increase the expression of APN and GLUT4mRNA, while AMPKα had no changes; PIP could increase thelevels of p-AMPKα and GLUT4protein expression, whereas no changes inAMPKα.ConclusionPIP could regulate APN, AMPKα and GLUT4of AMPK signaling pathway,which may be main possible reasons in improving glucose metabolism and insulinresistance.