Dietary intervention enhances fertility in obese male mice by regulating SLC2As.

IF 2.9 4区 生物学 Q3 CELL BIOLOGY
Liujia Sun, Xiaoqi Hong, Qi Zhu, Yu Xiang, Cen Xu, Lingling Weng, Jieyu Cai, Na Liang, Mingrui Xue, Hongshan Ge
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Abstract

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.

饮食干预通过调节SLC2As提高肥胖雄性小鼠的生育能力。
研究表明,肥胖会影响男性的生育能力和生殖潜力,但其潜在机制尚不清楚。本研究旨在探讨高脂肪饮食(HFD)和饮食干预对雄性小鼠生殖功能、葡萄糖代谢和相关SLC2As的影响。选取40只4周龄雄性ICR小鼠,随机分为正常饮食组(N组,N = 15)和高脂饮食组(F组,N = 25)。12周后,将小鼠进一步分为ND维持组(NN组,n = 10)、HFD维持组(FF组,n = 10),通过饮食干预8周转入ND组(FN组,n = 10)。进行腹腔葡萄糖耐量试验(IPGTT),记录空腹血糖、体重、精子数量、精子活力、睾丸和附睾等参数。苏木精-伊红染色观察睾丸形态。采用Western blot和免疫荧光法检测睾丸组织中SLC2As蛋白的表达和定位。长期消耗HFD导致体重和睾丸重量增加,睾丸和附睾器官系数降低,精子运动率降低,IPGTT试验曲线下面积增加。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SLC2A3和SLC2A8蛋白表达水平降低,FN组SLC2A8蛋白表达水平降低。HFD诱导的肥胖对雄性小鼠生殖系统造成损伤,影响睾丸糖代谢和糖转运体SLC2As的表达。从HFD到ND的转变可以在一定程度上改善膳食肥胖引起的生殖功能障碍及其对糖转运蛋白表达的影响。
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来源期刊
Journal of Molecular Histology
Journal of Molecular Histology 生物-细胞生物学
CiteScore
5.90
自引率
0.00%
发文量
68
审稿时长
1 months
期刊介绍: The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.
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