The effect of diabetes mellitus on endocrine and reproductive function.

The adverse effects of diabetes on the circulatory, visual, renal, and peripheral nervous system are commonly recognized and have been extensively studied. The effects of decreased insulin secretion or resistance to insulin action on endocrine glands have not been as carefully documented. Both clinical and animal research have demonstrated that diabetes mellitus is commonly associated with altered thyroid, adrenal and gonadal function. Some of these changes are reversed with insulin replacement therapy, but endocrine function is not always restored to normal even with rigorous glycemic control. Patients with poorly controlled diabetes exhibit basal and stimulated growth hormone (GH) hypersecretion, while patients with good metabolic control still present with diurnal and exercise-induced GH hypersecretion. In contrast, diabetes suppresses GH secretion in the rat. It is unclear why GH secretion is altered, but clinical and experimental evidence exists for diabetes-associated changes in GH-releasing hormone and somatostatin release as well as for changes in the pituitary response to these hypothalamic hormones. The thyroid hormones, T3 and T4, are usually suppressed in both humans and experimental animals with diabetes. This effect of diabetes appears to involve changes in hypothalamic thyrotropin-releasing hormone (TRH) secretion as well as changes in pituitary thyrotropin (TSH) release and direct effects at the level of the thyroid gland. Adrenal cortical function is often enhanced in diabetes, most likely due to alterations in glucocorticoid feedback responses. There is much conflicting data on adrenal medullary function in diabetes; responses to stress and exercise, however, are often abnormal. Finally, male and female reproductive function is often disrupted in diabetes. Data from animal studies suggest that the major cause is altered hypothalamic LHRH secretion secondary to diabetes-induced changes in hypothalamic neurotransmitter metabolism.