Yi Xuejie, Gao Haining, Chen Dequan, Tang Donghui, Huang Wanting, Li Tao, Ma Tie, Chang Bo
Department of Kinesiology, Shenyang Sport University, Shenyang, Liaoning, China.
Department of Physical Education, Minnan Normal University, Zhangzhou, Fujian, China; and.
Am J Physiol Regul Integr Comp Physiol. 2017 Apr 1;312(4):R501-R510. doi: 10.1152/ajpregu.00405.2016. Epub 2017 Jan 18.
To explore the role of the testicular leptin and JAK-STAT[leptin (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 and high-fat diet groups. After 10 wk, mice in the high-fat diet-fed group were further divided randomly into obese control, obese moderate-volume exercise, and obese high-volume exercise groups. Mice in the obese moderate-volume exercise group were provided with 2 h/day, 6 days/wk swimming exercise for 8 wk, and mice in the obese high-volume exercise group underwent twice the amount of daily exercise intervention as the obese moderate-volume exercise group. The results showed that a high-fat diet causes obesity, leptin resistance, inhibition of the testicular LEP-JAK-STAT pathway, decreased mRNA and protein expression of steroidogenic factor-1, steroidogenic acute regulatory protein, and the -450 side-chain cleavage enzyme, a decrease in the serum testosterone-to-estradiol ratio, and declines 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 steroidogenic factor-1, steroidogenic acute regulatory protein, and -450 side-chain cleavage enzyme and significantly reversed the serum testosterone-to-estradiol 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.
为了探究睾丸瘦素和JAK-STAT[瘦素（LEP）-JAK-STAT]通路在幼年阶段睾酮生物合成及减肥运动中的作用，将雄性C57BL/6J小鼠随机分为正常饮食组和高脂饮食组。10周后，高脂饮食喂养组的小鼠进一步随机分为肥胖对照组、肥胖中等运动量运动组和肥胖大运动量运动组。肥胖中等运动量运动组的小鼠每天进行2小时、每周6天的游泳运动，持续8周，肥胖大运动量运动组的小鼠每天运动干预量是肥胖中等运动量运动组的两倍。结果表明，高脂饮食会导致肥胖、瘦素抵抗、睾丸LEP-JAK-STAT通路受到抑制、类固醇生成因子-1、类固醇生成急性调节蛋白和细胞色素P450侧链裂解酶的mRNA和蛋白表达降低、血清睾酮与雌二醇比值下降以及精子质量参数降低。中等运动量和大运动量运动均能减少体脂并增加LEP-JAK-STAT的mRNA和蛋白表达，但只有中等运动量运动能显著增加类固醇生成因子-1、类固醇生成急性调节蛋白和细胞色素P450侧链裂解酶的mRNA和蛋白表达，并显著逆转血清睾酮与雌二醇比值及精子质量参数。这些发现表明，早期肥胖通过损害睾丸LEP-JAK-STAT通路抑制睾酮的生物合成和性发育，并降低雄性生殖潜能。长期的中等运动量和大运动量运动可有效减少体脂并改善肥胖引起的睾丸瘦素信号转导异常，而只有中等运动量运动能逆转肥胖对雄性生殖功能的负面影响。
