Selenoprotein SelK increases the secretion of insulin from MIN6 β cells

Abstract

The trace element selenium has an insulin-like effect on humans and animals. In this study, the effect and mechanism of mouse selenoprotein K (mSelK) on the secretion of insulin from mouse MIN6 β cells were investigated. An adenovirus vector, Ad-mSelK, was used to over-express the mSelK gene in the MIN6 β cells. Likewise, a lentivirus vector, LV-mSelK-RNAi, was used to knockdown mSelK expression in the MIN6 β cells. It was shown that the over-expression/knockdown of mSelK could increase/decrease the insulin secretion from MIN6 β cells. Meanwhile, the cytosolic free Ca²⁺ level and inositol trisphosphate receptor type 3 (IP3R3) expression were also increased/decreased significantly as a consequence of the over-expression/knockdown of mSelK in MIN6 β cells. Over-expression/knockdown of mSelK did not affect the expression of glutathione peroxidase 1 (GPx1) in the MIN6 β cells. Further studies revealed that the mSelK expression and insulin release levels were increased significantly by treatment of MIN6 β cells with selenium supplement (sodium selenite, Na₂SeO₃). In addition, mSelK protein levels were also up-regulated significantly in MIN6 β cells by adding glucose. These results suggest that mSelK plays a vital role in the process of trace element selenium promoting the secretion of insulin from MIN6 β cells. The expression of mSelK may increase the secretion of insulin by improving the expression of IP3R3 on the endoplasmic reticulum (ER), which elevated the cytosolic free Ca²⁺ level by enhancing the release of Ca²⁺ from the ER.