Mechanism of bromocriptine-induced hyperglycaemia

Abstract

Results reveal that bromocriptine at a dose of 6 mg/kg. I.P. in mice caused a significant hyperglycaemic effect which was accompanied by a marked increase in liver glycogen. After adren̂alectomy, the effect of bromocriptine on serum glucose level was reduced whereas its effect on liver glycogen content was abolished. In rats, administration of bromocriptine (17.5 mg/kg I.P.) induced a significant rise in serum glucose level which was associated with marked reduction in serum insulin activity and increase in serum corticosterone level with no effect on serum triiodothyronine (T3) or thyroxine (T4) levels. It could be concluded that bromocriptine-induced hyperglycaemia might be attributed at least partially to inhibition of insulin release and stimulation of corticosterone secretion. Previous studies disclosed that bromocri tine produced a marked hyperglycaemic effect in mice (1). This effect could be correlated with insulin secretion since bromocriptine was shown to inhibit glucose-stimulated insulin release by mouse pancreatic islets (2,3). In the present study, the effect of bromocriptine on the serum levels of insulin and corticosterone was investigated in an attempt to explain the mechanism of hyperglycaemia caused by bromocriptine. Our results indicate that bromocriptine-induced hyperglycaemia was accompanied by a significant inhibition of serum insulin level and marked elevation in serum corticosterone level in rats. The hyperglycaemic effect was reduced by adrenalectomy.