Voluntary exercise improves sperm parameters in high fat diet receiving rats through alteration in testicular oxidative stress, mir-34a/SIRT1/p53 and apoptosis.

Abstract

High fat diet can lead to testicular structural and functional disturbances, spermatogenesis disorders as well as infertility. So, the present investigation was proposed to clarify whether voluntary exercise could prevent high fat diet induced reproductive complications in rats through testicular stress oxidative and apoptosis. Forty male Wistar rats were randomly divided into four groups; control (C), voluntary exercise (VE), high fat diet (HFD) and high fat diet and voluntary exercise (VE+HFD) groups. The rats in the VE and VE+HFD groups were accommodated in apart cages that had running wheels and the running distance was assessed daily for 10weeks. In VE+HFD group, animals were fed with HFD for five weeks before commencing exercise. The sperm parameters, the expressions of testicular miR-34a gene, and P53 and SIRT1 proteins as well as testicular apoptosis were analyzed in all groups. The results indicated that voluntary exercise in VE+HFD group led to significantly increased GPX and SOD activities, SIRT1 protein expression, sperm parameters, and decreased the expression of miR34a gene and Acp53 protein, and cellular apoptosis index compared to HFD group (p<0.001 to p<0.05). The SOD and catalase activities, SIRT1 protein expression, sperm parameters in VE+HFD group were lower than of those of VE group, however, MDA content, expression of Acp53 protein, apoptosis indexes in VE+HFD group was higher than that of VE group (p<0.001 to p<0.05). This study revealed that voluntary exercise improved spermatogenesis, in part by decreasing the testicular oxidative stress status, apoptosis through alteration in miR-34a/SIRT1/p53 pathway.