In male rats, experimentally induced diabetes mellitus has been reported to be associated with reduced serum levels of gonadotropins and testosterone as well as decreased sex accessory organ weights. The purpose of the present study was to determine if the decreased accessory organ weights and gonadotropin levels observed in diabetic animals result from alterations in the ability of target tissues to respond to testosterone. Adult, male, Wistar rats were injected with streptozotocin (STZ) and either maintained as untreated diabetics or treated with daily injections of insulin. Semi-starved animals were included to control for any effects on the reproductive system due to body weight change alone. These three groups, plus intact controls, were maintained for 30 days with one-half of the animals from each group receiving silastic tubing implants of testosterone of various lengths. It was determined that, in uncontrolled diabetic and semi-starved animals, the serum levels of LH, FSH, and testosterone were decreased, as were the weights of seminal vesicles and ventral prostate glands. Insulin treatment restored LH, FSH, and testosterone levels to normal. Sex accessory glands exhibited slight, but significant, recovery in diabetic animals treated with insulin. Implants of testosterone that resulted in physiologic serum levels of testosterone were effective in depressing serum LH and FSH levels as well as in maintaining normal seminal vesicle and ventral prostate weights in control and semi-starved animals. In contrast, the diabetic animals did not respond to testosterone by either inhibition of gonadotropin release or maintenance of sex accessory weights. Insulin-maintained diabetic animals exhibited normal response to testosterone in terms of gonadotropin release; however, insulin treatment had only marginal effects on the response of sex accessory organs. The inability of testosterone to inhibit gonadotropin release or stimulate growth of sex accessory organs in diabetic rats may indicate that a primary reason for reproductive dysfunction in the experimentally induced, diabetic male rat is due to altered actions or accessibility of androgene at the level of the steroid target tissues.

This content is only available via PDF.