SHIP2 on pI3K/Akt pathway in palmitic acid stimulated islet β cell.

This study is to investigate the influence of SHIP2 on palmitic acid stimulated islet β cell and insulin secretion, as well as its role in pI3K/Akt pathway. We defined four groups: control, acid group, acid + NC siRNA group and acid + siRNA transfection group. The control was neither treated by palmitic acid nor transfection. The acid group was subjected to palmitic acid incubation. The acid + NC siRNA group was transiently transfected by NC siRNA, then was stimulated by palmitic acid. The acid + siRNA group was transiently transfected by siRNA, then was stimulated by palmitic acid. Cell proliferation and apoptosis were measured by MTT and flow cytometry. Immunocytochemistry, Western Blot and QPCR were designed to detect the expression of SHIP2, Akt, p-Akt protein and mRNA. Insulin secretion was tested by radioimmunoassay. The apoptosis rate in the acid + siRNA group was non-significantly lower than the acid group and the acid + NC siRNA group (P > 0.05). The expression levels of Akt phosphorylation in the acid + siRNA group was significantly higher than in the acid + NC siRNA group and the acid group (P < 0.05). And under 22.4 mmol/L glucose KRB, insulin secretion in the acid + siRNA group was significantly more than the acid + NC siRNA group and the acid group (P < 0.05). SHIP2 silencing probably stimulates insulin secretion, which may be associated with the enhanced proliferation in the pI3K/Akt pathway.