Primary Hypoandrogenism in Experimental Diabetes in the Long-Evans Rat

The hormonal milieu of the testis was examined in streptozocin-induced diabetic (STZ-D) adult male Wistar and Long-Evans rats. Serum testosterone, creatinine, and urea nitrogen (BUN) levels and blood glucose concentrations were determined in diabetic and control Wistar rats (experiment 1). These parameters plus luteinizing hormone (LH) and folliclestimulating hormone (FSH) levels were studied in experiments 2 and 3 with Long-Evans rats in untreated diabetic, control, insulin-treated diabetic, nondiabetic STZ-injected, and semistarved groups. Wistar diabetic rats had significantly decreased serum testosterone and increased blood glucose, BUN, and serum creatinine compared with controls. Several findings in Long-Evans rats suggested the existence of a primary Leydig cell defect in steroidogenesis during untreated diabetes that was completely or partially compensated for by increased pituitary gonadotropin secretion. Serum LH and FSH levels increased in Long-Evans diabetic rats. Serum testosterone was significantly reduced only in experiment 2. These hormonal alterations from control levels were not seen in insulin-treated diabetic animals. Semistarved animals, weight matched to the diabetic group in experiment 2, had significantly decreased serum testosterone and increased FSH levels. In addition, Long-Evans diabetic rat BUN and serum creatinine levels increased much less or were unchanged from control values compared with the increase noted in diabetic Wistar rats. In light of the hypogonadism that complicates clinical uremia, these findings suggest the more apt use of the Long- Evans strain rather than the Wistar strain in the study of STZ-D hypogonadal function. Indices to evaluate fertility (sperm count and motility) in diabetic rats in experiment 3 showed no change from those determined in control animals. The same diabetic animals, however, had a complete lack of reproductive success after pairing with cycling control females. These latter findings suggested that, in addition to a primary Leydig cell defect and resulting lowered testosterone, other factors may have contributed to the reproductive dysfunction of Long-Evans male rats with STZ-D.