毛螺菌科
生产过剩
肠道菌群
脂质代谢
脂肪酸
肥胖
新陈代谢
大肠杆菌
共生
生物
微生物学
细菌
生物化学
遗传学
基因
内分泌学
16S核糖体RNA
厚壁菌
作者
Tadashi Takeuchi,Keishi Kameyama,Eiji Miyauchi,Yumiko Nakanishi,Takashi Kanaya,Takayoshi Fujii,Tamotsu Kato,Takaharu Sasaki,Naoko Tachibana,Hiroki Negishi,Misato Matsui,Hiroshi Ohno
出处
期刊:Cell Metabolism
[Elsevier]
日期:2023-01-17
卷期号:35 (2): 361-375.e9
被引量:61
标识
DOI:10.1016/j.cmet.2022.12.013
摘要
Although recent studies have highlighted the impact of gut microbes on the progression of obesity and its comorbidities, it is not fully understood how these microbes promote these disorders, especially in terms of the role of microbial metabolites. Here, we report that Fusimonas intestini, a commensal species of the family Lachnospiraceae, is highly colonized in both humans and mice with obesity and hyperglycemia, produces long-chain fatty acids such as elaidate, and consequently facilitates diet-induced obesity. High fat intake altered the expression of microbial genes involved in lipid production, such as the fatty acid metabolism regulator fadR. Monocolonization with a FadR-overexpressing Escherichia coli exacerbated the metabolic phenotypes, suggesting that the change in bacterial lipid metabolism is causally involved in disease progression. Mechanistically, the microbe-derived fatty acids impaired intestinal epithelial integrity to promote metabolic endotoxemia. Our study thus provides a mechanistic linkage between gut commensals and obesity through the overproduction of microbe-derived lipids.
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