- Takashi Toyama (Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University / email@example.com)
- Yoshiro Saito (Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University / firstname.lastname@example.org)
Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University
We’ve previously shown that high levels of selenoprotein P (SeP), a major selenoprotein in plasma, can be a risk factor of type 2 diabetes. It was also thought that inhibition of insulin secretion caused by over-supplementation of selenium by SeP to pancreatic β cells contributed to the progress of diabetes. On the other hand, methylmercury, which is an environmental pollutant, is known to cancel the action of selenium via the covalent modification. Therefore, we thought that the interaction between selenium and methylmercury could be associated with the pathogenesis of diabetes. To address the hypothesis, MIN6 cells, a mouse pancreatic β-cell line, were treated with selenocystine (as a selenium donner) and methylmercury then examined insulin release from the cells. Selenocystine (400–1200 nM), which corresponds to the concentration of selenium in SeP of diabetic patients, shows cytotoxicity and inhibited glucose-driven insulin secretion. Methylmercury rescued the cytotoxicity that induced by selenocystine, however it affected the insulin secretion that is depressed by selenocystine at little intense. These data indicate that the mechanisms underlying inhibition of insulin secretion by selenocystine are independent of cytotoxicity, and methylmercury cannot be expected to restore insulin secretion or suppress diabetes as selenium neutlizer.