Effects of obesity and exercise on testicular leptin signal transduction and testosterone biosynthesis in male mice
Effects of obesity and exercise on testicular leptin signal transduction and testosterone biosynthesis in male mice
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肥胖和运动对雄性小鼠睾丸瘦素信号转导和睾酮生物合成的影响
DOI：
10.1152/ajpregu.00405.2016
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发表时间：
2017-04-01
影响因子：
2.8
通讯作者：
Chang, Bo
中科院分区：
文献类型：
--
作者：
Yi, Xuejie;Gao, Haining;Chang, Bo
为探讨睾丸瘦素（leptin）和JAK-STAT[leptin（LEP）-JAK-STAT]通路在幼年期睾酮合成和运动减肥中的作用，将雄性C57 BL/6 J小鼠随机分为正常饮食组和高脂饮食组。10 wk后，将高脂饲料喂养组小鼠随机分为肥胖对照组、肥胖中等量运动组和肥胖大量运动组。肥胖中量运动组进行2 h/d、6 d/wk的游泳运动，共8 wk;肥胖大量运动组进行2倍于肥胖中量运动组的运动干预。结果表明，高脂饮食导致肥胖、瘦素抵抗、睾丸LEP-JAK-STAT通路抑制、类固醇生成因子-1、类固醇生成急性调节蛋白和P-450侧链裂解酶的mRNA和蛋白表达降低、血清睾酮/雌二醇比值降低以及精子质量参数下降。中等和高负荷运动均能降低体脂并增加LEP-JAK-STAT的mRNA和蛋白表达，但只有中等负荷运动显著增加类固醇生成因子-1、类固醇生成急性调节蛋白和P-450侧链裂解酶的mRNA和蛋白表达，并显著逆转血清睾酮/雌二醇比值和精子质量参数。这些发现表明，通过损害睾丸LEP-JAKSTAT通路，早期肥胖抑制睾酮的生物合成和性发育，并降低男性生殖潜力。长期的中、大负荷运动能有效降低体脂，改善肥胖引起的睾丸瘦素信号转导异常，而只有中等负荷运动才能逆转肥胖对男性生殖功能的负面影响。
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 P-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 P-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-JAKSTAT 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.