减少AdipoR1信号传递及其对肥胖引起的男性不孕症的影响
Toshiko Kobori1, Masato Iwabu2,3, Miki Okada-Iwabu4,5
1Division of Diabetes and Metabolism, The Institute of Medical Science, Asahi Life Foundation, Chuo-Ku, Tokyo, 103-0002, Japan.
Scientific reports
|March 8, 2024
概括
肥胖会通过降低精子质量来损害男性的生育能力. 减少丸中的AdipoR1/AMPK信号增加了细胞亡,导致不孕. 在肥胖小鼠中,AdipoRon治疗改善了精子运动性.
科学领域:
- 生殖生物学 生殖生物学
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 肥胖是男性不孕症的一个已知的危险因素,但确切的机制仍然不完全理解.
- 现有研究表明,有几个途径将肥胖与男性不孕能力联系在一起,需要进一步调查分子基础.
研究的目的:
- 阐明阿迪波R1 (阿迪波内克丁受体1) 信号在肥胖引起的男性不孕症中的作用.
- 调查阿迪波R1缺乏对丸功能和精子参数的影响.
- 评估AdipoRon在缓解与肥胖相关的男性不孕症方面的治疗潜力.
主要方法:
- 在雄性小鼠中高脂肪饮食诱导的肥胖模型.
- 对精子数量,运动性和受精能力的分析.
- 在丸组织中评估AdipoR1基因和蛋白质表达.
- 评估亡标记物,包括caspase-6活性和亲亡基因表达.
- 使用AdipoR1淘汰赛小鼠和AdipoRon的使用.
主要成果:
- 吃高脂肪饮食的雄性小鼠表现出精子数量,运动性和受精能力的下降,以及阿迪波R1表达的减少和丸中亡的增加.
- 与野生类型对照组相比,AdipoR1淘汰小鼠的丸重量,精子参数和AMPK酸化显著降低,亡标志物增加.
- 口服AdipoRon通过降低caspase-6活性和丸亡,改善了肥胖小鼠的精子运动性.
结论:
- 丸中的AdipoR1/AMPK信号减少有助于增加caspase-6活性和亡,可能导致肥胖引起的男性不孕症.
- 阿迪波R1在维持丸功能和精子质量方面发挥着至关重要的作用.
- 阿迪波龙显示出治疗男性不孕症的治疗潜力,与肥胖症和AdipoR1信号受损相关.
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