Diabetes was induced in adult male albino rats by a single intravenous injection of streptozotocin (75 mg/kg body weight). The diabetes was allowed to stabilize for at least 15 days, whereafter the testicular and seminal vesicle histology was studied at various time intervals. Reduction in testis weights and tubule diameters was significant after 2 weeks of diabetes. The changes in seminiferous tubules ranged from premature sloughing of epithelium to total cessation of spermatogenesis. The testicular histology of diabetic animals frequently greatly simulated the situation described following hypophysectomy. By subjective visual assessment the number of Leydig cells was found to be normal or reduced in all of the diabetic animals. Diabetes was also demonstrated to induce seminal vesicle atrophy, which did not show any correlation with the degree of testicular lesions. The possible etiology of testicular damage in diabetic animals is discussed.

The uptake and retention of 1, 2-³H-testosterone in accessory sex glands, muscle and liver of streptozotocin diabetic castrated male rats, insulin-treated diabetic castrated rats and non-diabetic castrated control rats were studied at various time intervals after an intravenous injection. Diabetes reduced the retention of ³H-testosterone in the prostate, the preputial gland and the epididymis. Exogenous insulin slightly increased the retention of ³H-testosterone in these tissues of diabetic rats. No significant differences in the radioactivity in the rectus abdominis muscle, the coagulating glands and the seminal vesicles were found between the various experimental groups. Ventral prostate homogenates obtained from diabetic and control rats were incubated with ³H-testosterone in vitro. The steroids were extracted and thin-layer chromatographs were scanned for radioactivity. In prostatic homogenates taken from diabetic rats, testosterone transformation to dihydrotestosterone was reduced. The results indicate that the impaired function and androgen retention of the accessory sex glands of diabetic male rats is at least partly due to the reduced formation of dihydrotestosterone from testosterone.

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