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DOI | 10.1126/science.aba3683 |
High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide | |
Woongjae Yoo; Jacob K. Zieba; Nora J. Foegeding; Teresa P. Torres; Catherine D. Shelton; Nicolas G. Shealy; Austin J. Byndloss; Stephanie A. Cevallos; Erik Gertz; Connor R. Tiffany; Julia D. Thomas; Yael Litvak; Henry Nguyen; Erin E. Olsan; Brian J. Bennett; Jeffrey C. Rathmell; Amy S. Major; Andreas J. Bäumler; Mariana X. Byndloss | |
2021-08-13 | |
发表期刊 | Science
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出版年 | 2021 |
英文摘要 | What people eat has an immediate selective effect on the microbial populations resident in the gut. A high-fat diet is associated with the occurrence of microbes that catabolize choline and the accumulation of trimethylamine N -oxide (TMAO) in the bloodstream, a contributing factor for heart disease. Yoo et al. explored the microbial organisms and pathways that convert choline into TMAO in mice. Although gene clusters for choline metabolism are found widely among the microbiota, it is only the facultative anaerobes that become abundant in hosts on a high-fat diet. A high-fat diet impairs mitochondrial uptake of oxygen into host enterocytes and elevates nitrate in the mucus, which in turn weakens healthy anaerobic gut function. Facultative anaerobes such as the pathobiont Escherichia coli become dominant, which leads to an overall increase in the amount of choline catabolized into the precursor for TMAO. Whether this pathway plays a role in heart disease remains unclear. Science , aba3683, this issue p. [813][1] A Western-style, high-fat diet promotes cardiovascular disease, in part because it is rich in choline, which is converted to trimethylamine (TMA) by the gut microbiota. However, whether diet-induced changes in intestinal physiology can alter the metabolic capacity of the microbiota remains unknown. Using a mouse model of diet-induced obesity, we show that chronic exposure to a high-fat diet escalates Escherichia coli choline catabolism by altering intestinal epithelial physiology. A high-fat diet impaired the bioenergetics of mitochondria in the colonic epithelium to increase the luminal bioavailability of oxygen and nitrate, thereby intensifying respiration-dependent choline catabolism of E. coli . In turn, E. coli choline catabolism increased levels of circulating trimethlamine N -oxide, which is a potentially harmful metabolite generated by gut microbiota. [1]: /lookup/doi/10.1126/science.aba3683 |
领域 | 气候变化 ; 资源环境 |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/335890 |
专题 | 气候变化 资源环境科学 |
推荐引用方式 GB/T 7714 | Woongjae Yoo,Jacob K. Zieba,Nora J. Foegeding,等. High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide[J]. Science,2021. |
APA | Woongjae Yoo.,Jacob K. Zieba.,Nora J. Foegeding.,Teresa P. Torres.,Catherine D. Shelton.,...&Mariana X. Byndloss.(2021).High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide.Science. |
MLA | Woongjae Yoo,et al."High-fat diet–induced colonocyte dysfunction escalates microbiota-derived trimethylamine N-oxide".Science (2021). |
条目包含的文件 | 条目无相关文件。 |
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