Effect of Visfatin on Testosterone Hormone Level in Chronic Restraint Male Albino Rats
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- Category: Vol. 86, December 2018
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Effect of Visfatin on Testosterone Hormone Level in Chronic Restraint Male Albino Rats, RADWA M. AL-SAYED and SAFYA E. ESMAEEL
Abstract
Background: Stress has been linked in many studies with infertility and hormonal irregularities. Visfatin is a novel adipocytokine which has been proven to decrease in chronic stress in rats.
Aim of Study: This study aimed at evaluation of the effect of visfatin in modulation of the complications of chronic restraint on gonadal functions.
Material and Methods: 32 male albino rats randomly allocated to four equal groups, group (I): Included rats fed a normal diet (control group) group (II): Included rats fed a normal diet for 2 months then received a single intraperitoneal 500pmol visfatin injection group (III): Included immobilized rats (4hr/day) for 2 months and group (IV): Included immo-bilized rats (4hr/day) for 2 months then received a single intraperitoneal visfatin injection at a dose of 500pmol. After the last visfatin dose blood samples were collected and exam-ined for testosterone, LH and FSH. Then laparotomy was conducted to dissect the right testis for histopathological studies.
Results: The restraint stress has inhibitory effects on male testosterone, LH, FSH and testicular tissues in rats, marked deterioration of gonadal functions in immobilization stress group (group III), a significant decrease (p<0.001) in serum testosterone, LH, sperm count and right testicular weights, marked deterioration in the gonadal histoarchitecture, but, there was a non-significant change in serum FSH. Exogenous visfatin administration in (group IV) significantly increased serum testosterone (p<0.01), LH (p<0.001), FSH (p<0.01), and sperm count (p<0.001) than group III, and markedly improved the gonadal histoarchitecture. Group II demonstrated results similar to group III when compared to the control group.
Conclusion: Visfatin plays a protective role against chronic stress-induced gonadal dysfunction via maintaining testicular steroidogenesis of Leydig cells.