Abstract
Physiology department-Faculty of medicine-Zagazig University Abstract Background: Oxidative stress is increased in Diabetes mellitus (DM). Ghrelin is a peptide hormone produced by different tissues and its circulating level is decreased in type 1 DM. Recently, it has been shown to have antioxidant properties. Objective: This study is designed to investigate the effects of diabetes mellitus on testicular functions and the role of ghrelin in the modulation of these effects in a rat model of type 1 diabetes mellitus induced by Streptozotocin. Materials and methods: 32 healthy adult albino male rats of 170-195 gm initial body weight were utilized. The Rats were randomly and equally divided into 4 groups, group (1a): Vehicle treated (control) group, group (1b): Ghrelin treated normal group, group (IIa): STZ-diabetic group and group (IIb): Ghrelin treated diabetic group. Rats were weighed and checked for the serum levels of glucose, insulin, FSH, LH& testosterone levels, epididymal sperm count and motility, testicular malondialdhyde (MDA) level and superoxide dismutase (SOD), catalase (CAT) & glutathione peroxidase (GPX) activities and testicular weight & histopathology. Results and discussion: STZ-induced diabetes significantly decreased body weight, testes weight, serum insulin, FSH, LH & testosterone levels, epididymal sperm count & motility and testicular SOD, CAT & GPX activities. However, they significantly increased serum glucose & testicular malondialdhyde levels parallel with deterioration of the testicular histoarchitecture. In addition, it was found that exogenous administration of ghrelin resulted in a significant recovery of the above mentioned parameters in the diabetic group, while in the normal group, it was only associated with potentiating of the testicular antioxidant system as well as a significant increase in the body and testes weights. Conclusion: Ghrelin has a potential protective role against diabetes-induced pituitary testicular dysfunction which may be due to its antioxidant properties and maintenance of glucose and insulin homeostasis.
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