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Resveratrol appears to protect against oxidative stress and steroidogenesis collapse in mice fed high‐calorie and high‐cholesterol diet
Author(s) -
Wang H.J.,
Wang Q.,
Lv Z.M.,
Wang C.L.,
Li C.P.,
Rong Y.L.
Publication year - 2015
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.12231
Subject(s) - resveratrol , endocrinology , medicine , testosterone (patch) , oxidative stress , leydig cell , antioxidant , hormone , biology , pharmacology , luteinizing hormone , biochemistry
Summary The detrimental effects on Leydig cells steroidogenesis in mice on high‐calorie and high‐cholesterol diet ( HCD ) were determined, and the possible protection conferred by resveratrol supplementation was investigated. Male C 57 BL /6J mice were fed high‐calorie and alone ( HCD group) or with resveratrol supplementation ( HCD + Res group) for 18 weeks. Male C 57 BL /6J mice fed standard diet without or with the same dose of resveratrol served as controls. At the end of the experiment, there were significant declines of serum testosterone and luteinising hormone ( LH ) in HCD group as compared to controls. In line with the hormone alterations, the expressions of S t AR and steroidogenic enzymes in testicular tissues were significantly down‐regulated in HCD group. Resveratrol supplementation could significantly improve expressions of S t AR and steroidogenic enzymes, and increase serum testosterone and LH concentrations in HCD + Res group. Mice in HCD group also showed a statistically significant down‐regulation in the m RNA expressions of M n SOD and GP x4. Resveratrol supplementation improved testicular M n SOD and GP x4 expression in comparison with HCD group. We propose that resveratrol may attenuate detrimental effects on Leydig cells steroidogenesis in HCD ‐fed mice, and its upregulations of antioxidant defence mechanisms and LH level may play a role in its protection. Our data suggest resveratrol appears to have the potential for therapeutic approaches targeting male obesity‐associated secondary hypogonadism.