RESEARCH ARTICLE The Possible Mechanisms of the Impaired Insulin Secretion in Hypothyroid Rats

Although the insulin secretion deficit in hypothyroid male rats has been documented, the underling mechanisms of the effect of hypothyroidism on insulin secretion are not clear. Iso-lated islets of the PTU-induced hypothyroid and control rats were exposed to glibenclamide, acetylcholine, and nifedipine in the presence of glucose concentrations of 2.8 or 8.3 and 16.7 mmol/L. Glucokinase and hexokinase specific activity, glucokinase content, and glu-cose transporter 2 protein expression were also determined in the isolated islets. Isolated islets from the hypothyroid rats showed a defect in insulin secretion in response to high glu-cose. In the presence of glibenclamide or acetylcholine, the isolated islets from the hypothy-roid and control rats stimulated by glucose concentration of 16.7 mmol/L secreted similar amounts of insulin. In the presence of glucose concentrations of 8.3 mmol/L and 16.7 mmol/ L, nifedipine was able to diminish insulin secretion from isolated islets of both groups, indi-cating that probably the defect may not arise from L type calcium channels or the steps beyond depolarization or the elements involved in the acetylcoline signaling pathway. Glu-cokinase content and hexokinase specific activity were also the same in the control an