RESUMEN
BACKGROUND: Diabetes is a devastating metabolic disease that causes long-term damage to various organs. An important leading complication of diabetes is a degenerative effect on the reproductive system including infertility and gonadal dysfunction. This study aimed to evaluate the effects of experimental type I and II diabetes on the levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone. METHODS: Male Wistar rats were randomly divided into four separate groups: (1) type I diabetes (T1DM), (2) type II diabetes (T2DM), (3) cetrorelix acetate-treated nondiabetic control group, and (4) normal untreated group (n = 6). T1DM was experimentally induced by a single injection of alloxan (135 mg/kg) while T2DM was induced by feeding the animals with drinking water enriched with fructose (10%). Cetrorelix acetate (100 mg/kg, intraperitoneal for 1 week) treatment group was used as a positive control. All rats were killed and blood and testes were collected after 8 weeks of the study. The effects of induced diabetes on the levels of blood glucose and insulin were assessed. The levels of sex hormones and insulin were determined by radioimmunoassay. Histological staining was used to check abnormal patterns of testicular morphology, the diameter of seminiferous tubules, testicular diameter, and germinal layer thickness. RESULTS: A significant reduction in the testosterone, FSH, and LH levels were observed in T1DM, T2DM, and also in cetrorelix acetate-treated groups. Analysis of testicular histology sections revealed significantly reduced thickness of cell layer in T1DM and cetrorelix acetate-treated groups compared with the T2DM group. In T2DM, the cell numbers, the thickness of cell layer, the diameter of seminiferous tubules, and weight of testicles were slightly increased. In contrast, total tubules of empty seminiferous increased significantly in T1D and cetrorelix treated groups compared with the control group. CONCLUSION: Overall, diabetes can induce hypothalamus-pituitary-gonad axis dysfunction, affects hormonal secretion, and causes histological damage to testes, collectively leading to deleterious effects on male fertility.