Bromocriptine inhibits the seasonally occurring obesity, hyperinsulinemia, insulin resistance, and impaired glucose tolerance in the Syrian hamster, Mesocricetus auratus.

Seasonally obese-hyperinsulinemic female Syrian hamsters were injected daily with bromocriptine or saline for a period of 34 days to test for effects of bromocriptine on body fat store levels, hepatic triglyceride secretion, glucose tolerance, and plasma insulin and glucose concentrations. The effects of bromocriptine on body fat store levels, as well as on plasma insulin and glucose concentrations, in seasonally obese hamsters were compared with the levels of body fat, plasma insulin, and plasma glucose observed in seasonally lean hamsters. Bromocriptine treatment substantially improved glucose intolerance and reduced the total and stimulated areas under the glucose tolerance curve by 33% after 14 days of treatment. After 34 days of treatment, bromocriptine reduced body fat store levels by 36% and hepatic triglyceride secretion by 40% without any concurrent change in food consumption. Furthermore, bromocriptine reduced the plasma insulin level by 70%, while slightly reducing plasma glucose concentration (ie, 68% reduction in the insulin to glucose ratio). The reductions of body fat, plasma insulin, and plasma insulin to glucose ratio produced by bromocriptine in seasonally obese hamsters are equivalent to those observed in seasonally lean hamsters. Shifts in phase relationships of circadian neuroendocrine rhythms have been demonstrated to regulate annual cycles of metabolism in vertebrates, including the Syrian hamster. The effects of bromocriptine can also be explained as an alteration of such a circadian mechanism.