Molecular mechanism for berberine to improve insulin resistance in 3T3-L1 adipocytes / 中华内分泌代谢杂志

ABSTRACT

Objective To investigate the effect of berberine on insulin resistance induced by free fatty acid in 3T3-L1 adipocytes and the possible molecular mechanism.Methods 3T3-L1 adipocytes were treated with 0.5 mmol/L palmitic acid to induce insulin resistance.Berberine was used for treatment and aspirin for positive control.Glucose oxidase method was employed for measuring the glucose consumption in the medium and 2-deoxy- [~3H]-D-glucose method was used for the determination of glucose uptake.Western blot was used for the determination of IKB kinase(IKK)?SerlS1 phosphorylation,insulin receptor substrance-1(IRS-1)Ser307 phosphorylation,the protein expression of IKK?,IRS-1,phosphatidylinositol 3-kinase(PI-3K)p85 and glucose transporter 4(Glut4).Results After the treatment with 0. 5 mmol/L of palmitic acid for 24 h,glucose consumption by 3T3-L1 adipocytes was decreased by 41%,insulin-stimulated glucose transport was inhibited by 67%,IRS-1 and PI-3K p85 proteins were reduced, and phosphorylations of IKK?Ser181 and IRS-1 Ser307 were induced.The above results were reversed by adding berberine or aspirin.But Glut4 and IKK?protein abundance was not changed during this study.Conclusion Berberine significantly improves insulin resistance induced by free fatty acid in 3T3-L1 adipocytes via inhibiting IKK?serine phosphorylation.