肠道微生物群通过抑制 NLRP3/ASC/caspase-1 轴改善肥胖小鼠的生殖功能障碍。

IF 2.5 4区生物学 Q3 MICROBIOLOGY

Future microbiology Pub Date : 2024-01-01 Epub Date: 2024-09-03 DOI:10.1080/17460913.2024.2386867

Hui Huang, Ting Zhou, Feng He, Biao Wen, Ying Yang, Wei Zhong, Qiurong Wang, Jun Li

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引用次数: 0

摘要

目的：探讨肠道微生物群、肥胖相关的雄性生殖损伤和NLRP3炎性体之间的复杂关系：结果：高脂饮食诱导小鼠模型肥胖，粪便微生物群移植或高膳食纤维饮食（HDFD）持续5周，以评估小鼠生殖能力、NLRP3、肠道微生物群组成和代谢物相关参数的变化：结果：高脂肪饮食会诱发雄性小鼠肥胖并降低其生殖能力。粪便微生物群移植和高脂饮食可通过调整肠道微生物群来抑制 NLRP3/ASC/caspase-1 轴，从而降低 IL-1β 水平，从而提高肥胖小鼠的生殖能力：这项研究通过靶向肠道微生物群和 NLRP3 炎性体途径，为肥胖引起的生殖功能障碍提供了一种潜在的治疗方法。

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The gut microbiota improves reproductive dysfunction in obese mice by suppressing the NLRP3/ASC/caspase-1 axis.

Aim: To explore the complex relationship between gut microbiota, obesity-related male reproductive impairments, and the NLRP3 inflammasome.Methods: A high-fat diet was administered to induce obesity in a mouse model, fecal microbiota transplantation or a high-dietary fiber diet (HDFD) was administered for 5 weeks to evaluate changes in parameters related to reproductive capacity, NLRP3, gut microbiota composition and metabolites in mice.Results: A high-fat diet induces obesity and decreases reproductive capacity in male mice. Fecal microbiota transplantation and HDFD can improve reproductive capacity in obese mice by adjusting the gut microbiota population to suppress the NLRP3/ASC/caspase-1 axis, thereby reducing IL-1β levels.Conclusion: This study offers a potential treatment for obesity-induced reproductive dysfunction by targeting the gut microbiota and the NLRP3 inflammasome pathway.

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来源期刊

Future microbiology 生物-微生物学

CiteScore

4.90

自引率

3.20%

发文量

134

审稿时长

6-12 weeks

期刊介绍： Future Microbiology delivers essential information in concise, at-a-glance article formats. Key advances in the field are reported and analyzed by international experts, providing an authoritative but accessible forum for this increasingly important and vast area of research.