Expression and regulation of a two-pore domain K+ channel KCNK16 in rat islets

Abstract

Objective To observe the expression of a two-pore domain K+ channel KCNK16 in rat islets, and to explore its regulation by insulin secretagogues. Methods Real time-PCR and immunohistochemistry were employed to observe the expression of KCNK16 in rat islets and other tissues. Rat islets were exposed to glucose, prolactin, palmitate, and trichostatin A(TSA)for 24 h and KCNK16 expression were determined by realtime-PCR and Western blot. Glucose- and KCl-stimulated insulin secretion were assayed by ELISA after islets were exposed to TSA for 24 h. The dose- and time-dependent effects of TSA on KCNK16 expression in INS1-E cells were determined by RT-PCR. Results KCNK16 was highly expressed in rat islets. Glucose, prolactin, and palmitate did not affect the expression of KCNK16 in rat islets. TSA treatment significantly potentiated glucose- and KCl-stimulated insulin secretion in isolated rat islets(P<0.05), along with decreased KCNK16 mRNA and protein expressions(P<0.01). TSA inhibited KCNK16 expression in a dose- and time-dependent manner in INS1-E cells(P<0.05). Conclusion KCNK16 is exclusively and highly expressed in rat islets and its expression can be down-regulated by TSA treatment. It is possible that TSA enhances insulin secretion via decreasing KCNK16 expression. (Chin J Endocrinol Metab, 2015, 31: 452-456) Key words: KCNK16; Islet; Insulin secretion; Trichostatin A