Selenoprotein SelK increases the secretion of insulin from MIN6 beta cells

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 beta cells were investigated. An adenovirus vector, Ad-mSelK, was used to over-express the mSelK gene in the MIN6 beta cells. Likewise, a lentivirus vector, LV-mSelK-RNAi, was used to knockdown mSelK expression in the MIN6 b cells. It was shown that the over-expression/knockdown of mSelK could increase/decrease the insulin secretion from MIN6 beta 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 beta cells. Over-expression/knockdown of mSelK did not affect the expression of glutathione peroxidase 1 (GPx1) in the MIN6 beta cells. Further studies revealed that the mSelK expression and insulin release levels were increased significantly by treatment of MIN6 beta cells with selenium supplement (sodium selenite, Na2SeO3). In addition, mSelK protein levels were also up-regulated significantly in MIN6 beta 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 beta 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.