Sun Liujia, Hong Xiaoqi, Zhu Qi, Xiang Yu, Xu Cen, Weng Lingling, Cai Jieyu, Liang Na, Xue Mingrui, Ge Hongshan
Reproduction Medicine Centre, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, China.
Shaoxing People's Hospital, Shaoxing, China.
J Mol Histol. 2025 May 28;56(3):174. doi: 10.1007/s10735-025-10470-y.
Research has demonstrated that obesity can affect male fertility and reproductive potential, but the underlying mechanism remains unclear. This study aimed to investigate the effects of a high-fat diet (HFD) and dietary intervention on reproductive function, glucose metabolism, and related SLC2As in male mice. Forty 4-week-old male ICR mice were randomly divided into the normal diet (ND) group (group N, n = 15) and the HFD group (group F, n = 25). After 12 weeks, the mice were further divided into the following groups: ND maintenance group (NN group, n = 10), HFD maintenance group (FF group, n = 10), and transition to ND group (FN group, n = 10) through dietary intervention for 8 weeks. Intraperitoneal glucose tolerance test (IPGTT) was performed, and parameters including fasting blood glucose, body weight, sperm count, sperm motility, and testis and epididymis measurements were recorded. Testicular morphology was observed through hematoxylin-eosin staining. Western blot and immunofluorescence were used to detect the protein expression and localisation of SLC2As in the testis. Long-term HFD consumption resulted in increased body and testicular weights, decreased testicular and epididymal organ coefficients, reduced sperm motility rate, and increased area under the curve in the IPGTT test. After dietary intervention, compared to the NN group, the FF and FN groups exhibited increased testis weight, decreased testicular and epididymal organ coefficients, decreased sperm motility rate, reduced SLC2A3 and SLC2A8 protein expression levels in the FF group, and decreased SLC2A8 protein expression in the FN group. Obesity induced by HFD caused damage to the reproductive system of male mice and affected testicular glucose metabolism and the expression of sugar transporter SLC2As. Transitioning from HFD to ND can improve reproductive dysfunction caused by dietary obesity and its impact on sugar transporter protein expression to a certain extent.
研究表明，肥胖会影响男性生育能力和生殖潜能，但其潜在机制仍不清楚。本研究旨在探讨高脂饮食（HFD）和饮食干预对雄性小鼠生殖功能、糖代谢及相关溶质载体家族2成员A（SLC2A）的影响。将40只4周龄雄性ICR小鼠随机分为正常饮食（ND）组（N组，n = 15）和HFD组（F组，n = 25）。12周后，将小鼠进一步分为以下几组：ND维持组（NN组，n = 10）、HFD维持组（FF组，n = 10）以及通过8周饮食干预过渡到ND组（FN组，n = 10）。进行腹腔内葡萄糖耐量试验（IPGTT），并记录包括空腹血糖、体重、精子计数、精子活力以及睾丸和附睾测量值等参数。通过苏木精-伊红染色观察睾丸形态。采用蛋白质免疫印迹法和免疫荧光法检测睾丸中SLC2A的蛋白表达和定位。长期食用HFD导致体重和睾丸重量增加、睾丸和附睾器官系数降低、精子活力率降低以及IPGTT试验中曲线下面积增加。饮食干预后，与NN组相比，FF组和FN组睾丸重量增加、睾丸和附睾器官系数降低、精子活力率降低，FF组中溶质载体家族2成员A3（SLC2A3）和溶质载体家族2成员A8（SLC2A8）蛋白表达水平降低，FN组中SLC2A8蛋白表达降低。HFD诱导的肥胖对雄性小鼠生殖系统造成损害，并影响睾丸糖代谢和糖转运蛋白SLC2A的表达。从HFD过渡到ND可在一定程度上改善饮食性肥胖引起的生殖功能障碍及其对糖转运蛋白表达的影响。
