Myoinositol improves sperm parameters in diabetic rats by reducing oxidative stress and regulating apoptosis-related genes.

Diabetes disrupts spermatogenesis and leads to low-quality sperm by causing oxidative stress, inducing apoptosis and reducing testosterone level. Myoinositol has antiglycemic, antioxidant, anti-apoptotic, and testosterone-regulating properties. This study aimed to evaluate the potential of myoinositol in improving sperm production and sperm quality in diabetic rats. Eighteen rats were divided into three groups (n = 6 per group): control, diabetic (Streptozotocin + Nicotinamide), and diabetic + myoinositol supplementation (300 mg/kg, for 56 days). Sperm parameters, including count, total motility, viability, and morphology, were evaluated. Additionally, several biochemical and molecular markers were measured including serum malondialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (TAC), testosterone, Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), and Bax/Bcl2 gene expression ratio, Bax and Bcl2 protein expression, germinal epithelium apoptosis. In the diabetic group, sperm count, viability, and normal morphology significantly decreased, along with lower levels of SOD, TAC, testosterone, FSH, and LH. Conversely, MDA levels and the Bax/Bcl2 gene ratio significantly increased compared to the control group. In the diabetic + myoinositol group, sperm count, viability, morphology, and motility significantly improved (P < 0.001), as did TAC, testosterone, and FSH levels (P < 0.001), with a significant increase in LH levels (P < 0.05). Additionally, MDA levels (P < 0.01) and the Bax/Bcl2 gene ratio (P < 0.05) were significantly reduced compared to the diabetic group. This study showed that diabetes impairs sperm quality, antioxidant capacity, and hormones while increasing oxidative stress and apoptosis. Myoinositol improves sperm parameters, boosts antioxidants, and reduces apoptosis, suggesting its therapeutic potential for diabetes-induced reproductive dysfunction.