Effect of Streptozotocin-Diabetes and Insulin Treatment on Regulation of Leydig Cell Function in the Rat

Abstract

The present study was performed to further clarify the possible role played by insulin deficiency on the steroidogenic capacity of the rat testis. Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by i.p. injection (40 mg/kg b.w.) of streptozotocin and was monitored at 2-day intervals by measuring body weight and serum glucose, glucosuria and ketonuria levels. The effect of insulin therapy on pituitary LH content and plasma LH concentrations, as well as on the cyclic AMP level in interstitial cell incubation medium and plasma testosterone concentrations, was measured 30 days after the induction of diabetes by radioimmunoassay. Streptozotocin-induced diabetes resulted in significantly reduced pituitary LH (16%, P less than 0.025) and plasma LH (34%, P less than 0.02); insulin treatment completely restored these levels. Similarly, the cyclic AMP content of interstitial cell incubation medium and the plasma testosterone concentrations were dramatically decreased in the diabetic state (50%, P less than 0.005 and 63%, P less than 0.025, respectively) and combined treatment with insulin plus hCG appeared slightly more effective than treatment with either of these hormones alone, suggesting a possible synergistic action. It is concluded that decreased testicular steroidogenesis in the diabetic rat may represent, at least in part, a direct consequence of insulin deficiency at the hypothalamic and/or pituitary levels. However, our findings would also be consistent with other reports suggesting that insulin may play a direct role in the rat testis.

Endocrine profile and testicular histomorphometry in adult rat offspring of diabetic mothers

“…Levels of FSH, LH and testosterone in ODM were significantly lower than that of the control. A decrease in levels of FSH, LH, prolactin and growth hormone has been reported in diabetic rats [17,18]. Diabetes induces a decrease in the serum levels of LH, which is responsible for normal Leydig cell function (testosterone secretion) [18].…”

“…A decrease in levels of FSH, LH, prolactin and growth hormone has been reported in diabetic rats [17,18]. Diabetes induces a decrease in the serum levels of LH, which is responsible for normal Leydig cell function (testosterone secretion) [18]. The pituitary of diabetic rats has a blunted response, with a diminished stimuli-induced secretion of FSH and LH [24].…”

“…The follicle-stimulating hormone (FSH) regulates spermatogenesis, whereas the luteinizing hormone (LH) controls Leydig cell function. Decreases in the serum levels of FSH, LH, prolactin and growth hormone have been reported in diabetes [17,18]. The fetuses of diabetic mothers also experience hyperglycemia and hypoinsulinemia, which may have an adverse effect on their reproductive system (endocrine and testicular structure) during fetal development.…”

Poorly Controlled Type I Diabetes Mellitus in Young Men Selectively Suppresses Luteinizing Hormone Secretory Burst Mass

“…This central hypogonadotropism is paradoxically associated with the presence in the circulation of gonadotropin molecules with enriched biological activity, which is evidently sufficient to temporarily maintain normal total testosterone concentrations in the earlier stages of IDDM. (J Clin Endocrinol Metab 87: 5507-5515, 2002) I NSULINOPENIC DIABETES MELLITUS disrupts reproductive hormone outflow consistently in the experimental animal (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) and affects the gonadal axis to a variable extent in the human (15)(16)(17)(18)(19). For example, in the rodent, acute insulin withdrawal damps LH pulsatility and impairs acute gonadotrope secretory responsiveness to GnRH (10,13,14).…”

The Effect of the Aquatic Extract of Stevia on the MDA Level and Catalase Activity in the Testicular Tissue of Streptozotocin-Nicotinamide-Induced Diabetic Rats

“…MDA, as a product of lipid peroxidation, increases in diabetes; it is believed that MDA amplifies the damages of oxidative stress (31) (33). Overall, the excessive production of ROS leads to the inhibition of feedbacks and deactivation of oxidative enzymes; thus, SOD and CAT activity diminish (34).…”