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一种产丙酸的细菌,在高脂饮食诱导的小鼠肥胖中有助于GPR41信号传导和代谢调节。

, a propionate-producing bacterium, contributes to GPR41 signaling and metabolic regulation in high-fat diet-induced obesity in mice.

作者信息

Miyamoto Junki, Ando Yuna, Yamano Mayu, Nishida Akari, Murakami Kota, Kimura Ikuo

机构信息

Department of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu-shi, Tokyo, Japan.

Laboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan.

出版信息

Front Nutr. 2025 Apr 3;12:1542196. doi: 10.3389/fnut.2025.1542196. eCollection 2025.

Abstract

Obesity is a major healthcare problem worldwide and is induced by excess energy intake, resulting in gut microbial composition and microbial diversity changes. Through fermentation of dietary fibers, short-chain fatty acids (SCFAs) act as host energy sources and signaling molecules via G protein-coupled receptors such as GPR41. is widely used in many applications; however, studies on the beneficial effect of via propionate production and host energy homeostasis are unclear. Therefore, this study aimed to investigate the beneficial metabolic effects of by focusing on GPR41 signaling in a high-fat diet (HFD)-induced obesity mouse model. Here, we demonstrated that OB7439 improved host metabolism in HFD-induced obesity in mice. The intake of OB7439 improved metabolism in HFD-induced obese mice by increasing propionate production, regulating glucose tolerance, and inhibiting hepatic inflammation via GPR41 signaling. Our findings shed light on the potential of using OB7439 as an SCFA producer for the prevention and treatment of metabolic disorders. Based on these results, we suggest that may be a potential therapeutic bacterium that inhibits obesity and modulates the gut microbial community.

摘要

肥胖是全球主要的医疗保健问题,由能量摄入过多引起,导致肠道微生物组成和微生物多样性发生变化。通过膳食纤维的发酵,短链脂肪酸(SCFAs)作为宿主能量来源和信号分子,通过G蛋白偶联受体如GPR41发挥作用。 被广泛应用于许多领域;然而,关于 通过产生丙酸盐和宿主能量稳态的有益作用的研究尚不清楚。因此,本研究旨在通过关注高脂饮食(HFD)诱导的肥胖小鼠模型中的GPR41信号传导,研究 的有益代谢作用。在此,我们证明了 OB7439改善了HFD诱导的小鼠肥胖中的宿主代谢。摄入 OB7439通过增加丙酸盐产生、调节葡萄糖耐量和通过GPR41信号传导抑制肝脏炎症,改善了HFD诱导的肥胖小鼠的代谢。我们的研究结果揭示了使用 OB7439作为SCFA产生菌预防和治疗代谢紊乱的潜力。基于这些结果,我们认为 可能是一种潜在的治疗性细菌,可抑制肥胖并调节肠道微生物群落。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e240/12003125/58b4b1c27536/fnut-12-1542196-g001.jpg

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