To explore the role of the testicular leptin and JAK-STAT(LEP-JAK-STAT) pathway in testosterone biosynthesis during juvenile stages and exercise for weight loss, male C57BL/6J mice were randomly divided into normal-diet (ND) and high-fat diet (HFD) groups. After 10 weeks, mice in the HFD group were further divided randomly into obese control (OC), obese moderate-volume exercise (OME), and obese high-volume exercise (OHE) groups. Mice in the OME group were provided with 2 h/day, 6 days/week swimming exercise for 8 weeks and mice in the OHE group underwent twice the amount of daily exercise intervention as the OME group. The results showed that high-fat diet causes obesity, leptin resistance, inhibition of the testicular LEP-JAK-STAT pathway, decreased mRNA and protein expression of SF-1, StAR, and P450scc, decrease in the serum T/E2 ratio, and decline in sperm quality parameters. Both moderate and high-volume exercise were able to reduce body fat and increase the mRNA and protein expression of LEP-JAK-STAT, but only moderate exercise significantly increased the mRNA and protein expression of SF-1, StAR, and P450scc, and significantly reversed the serum T/E2 ratio and sperm quality parameters. These findings suggest that by impairing the testicular LEP-JAK-STAT pathway, early-stage obesity inhibits the biosynthesis of testosterone and sexual development and reduces male reproductive potential. Long-term moderate and high-volume exercise can effectively reduce body fat and improve obesity-induced abnormalities in testicular leptin signal transduction, whereas only moderate-volume exercise can reverse the negative impacts of obesity on male reproductive function.
- high-fat diet-induced obesity
- LEP-JAK-STAT signaling pathway
- steroidogenic enzyme
- Copyright © 2017, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology