OBJECTIVETo investigate the effect of potassium channel opener (diazoxide) on the islet cells apoptosis and bcl-2 and bax gene expressions in diabetic rats.

METHODSIslet cell apoptosis was induced by intraperitoneal injection of streptozocin (STZ). The rats were randomly allocated into normal control group (NC group), diabetes mellitus group (DM group), and diazoxide group (DIA group), all treated with diazoxide for 4 weeks. During and after the treatment, the general state, body weight, fasting plasma glucose (FPG), food intake, and oral glucose tolerance of the rats were assessed. The expressions of Bcl-2 and Bax in rat islet cells were measured by immunohistochemistry, and the cell apoptosis was analyzed by TUNEL assay.

RESULTSCompared with the NC group, the rats in the DM group showed significantly decreased body weight (P<0.05), increased blood glucose at o and 120 min after oral glucose administration, decreased expressions of Bcl-2 (P<0.01), increased expression of Bax (P<0.01), and increased islet cell apoptosis (P<0.05). Diazoxide treatment significantly decreased the body weight (P<0.05), decreased the blood glucose, increased Bcl-2 expression (P<0.01), decreased Bax expression (P<0.05), and reduced the islet cell apoptosis (P>0.05) of the diabetic rats.

CONCLUSIONBy causing potassium channel opening, diazoxide can obviously improve the oral glucose tolerance, reduce the body weight, and up-regulate Bcl-2 and down-regulate Bax expression in diabetic rats. Diazoxide can also reduce the apoptosis of the islet cells in diabetic rats.