Prepubertal onset of obesity negatively impacts on testicular steroidogenesis in rats. (5th December 2016)

• Record Type: Journal Article
• Authors: Wagner, I.V.; Klöting, N.; Atanassova, N.; Savchuk, I.; Spröte, C.; Kiess, W.; Söder, O.; Svechnikov, K.
• Is Part Of: Molecular and cellular endocrinology. Volume 437(2016)
• Page Start: 154
• Page End: 162
• Publication Date: 2016-12-05
• Subjects: Obesity -- Testicular steroidogenesis -- Sex hormones -- TNFα; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2016.08.027
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Obesity is a global health problem and impacts negatively on levels of testosterone and quality of sperm production. At present little is known about mechanisms that attenuate testicular function in obese males. Our study characterized testicular steroidogenesis and explored levels of relevant paracrine and hormonal factors in rats with short- and long-term obesity. We have found that obesity state increased serum levels of estradiol and leptin in both groups of obese rats and inhibited the expression of StAR and Cyp11a1 associated with low levels of intratesticular testosterone in rats with long-term obesity. Further, long-term obesity reduced the number of Leydig cells, increased the testicular levels of the proinflammatory adipocytokine TNFα and the number of testicular macrophages. All together, our data indicate that long-term obesity may cause chronic inflammation in the testis and negatively impacts on Leydig cell steroidogenesis. Highlights: Diet-induced obesity increases serum levels of estradiol and leptin in male rats. Long-term obesity reduces number of Leydig cells and steroidogenic gene expression. Long-term obesity elevates the testicular TNFα and the number of macrophages.