Mammalian reproduction is dynamically regulated by the pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These hormones are synthesized in the pituitary gland following stimulation by the gonadotropin-releasing hormone (GnRH) and act by stimulating steroid production and gametogenesis in both males and females. Male adult Sprague-Dawley rats (120 - 140 g) were randomly divided into 7 groups. Group 1 > Control group; fed on normal rat pellets. Group 2 > Streptozotocin group; received a single dose IP injection of streptozotocin 45 mg/kg BW in Na+ citrate buffer pH 4.5. Group 3 > Streptozotocin-insulin treated group; received a single dose IP injection of streptozotocin as in group 2 above and treated with insulin sub-cutaneously. Group 4 > Streptozotocin-ginger treated group; received a single dose IP injection of streptozotocin as in group 2 above and treated with 500 mg/Kg Ginger extract orally. Group 5 > Insulin resistant group; fed ad libitum on a special diet containing 25% fructose mixed with 75% normal rat chow (w/w). Group 6 > Insulin resistant-pioglitazone treated group; fed ad libitum on a special diet as in group 5 above and treated with Pioglitazone 15 mg/kg orally. Group 7 > Insulin resistant-ginger treated group; fed ad libitum on a special diet as in group 4 above, and also treated with 500 mg/Kg Ginger extract orally. Hormonal and tissue biochemistry analyses revealed that both central and local mechanisms are implicated in the impairment of spermatogenesis by diabetes but the hypothalamo-pituitary testicular axis alteration might not likely have a major impact as the local defect on steroidogenesis in the testis. This local defect could also predispose to male hypogonadism, i.e. failure of gonadal function.