Dual Effects Of Metformin On MIN6Pancreaticβ Cells Through AMPK-Dependent Autophagy

Objective To investigate the effects of metformin in MIN6pancreatic β cells under normal and free fatty acid culture condition, and the underlying mechanism.Methods MIN6mouse β cells were exposed to the normal culture condition or high free fatty acid condition. Metformin, AICAR (activator of phospho-AMPK), compound C (Inhibitor of phospho-AMPK),3-MA (Inhibitor of autophagy) were then added into the cell culture media. CCK-8assay was used to observe the proliferation rate of MIN6cells. The apoptosis rate of the cells was detected by flow cytometry. The expressions of p-AMPK, AMPK, C-caspase3, LC3B-Ⅱ were detected by Western blot.Results1)Under normal culture condition, Cell apoptosis rate increased in metformin treated MIN6cells.2) Under palmitate culture condition, Metformin treated MIN6cells presented a lower apoptosis rate than the control cells.3) Under either culture condition, AICAR showed a similar effect on MIN6cells with metformin.4) Under either culture condition, both compound C and3-MA could inhibit the effect of metformin. Conclusion By activate the autophagy effect, metformin plays a dual roles in MIN6cells.