生物
免疫系统
炎症
肠道菌群
脂肪组织
肥胖
免疫学
全身炎症
内分泌学
作者
Devesha H. Kulkarni,Brigida Rusconi,Alexandria N. Floyd,Emer Joyce,Khushi B. Talati,Hrishi Kousik,Dereck Alleyne,David C.H. Harris,Lorena Garnica,Ryan McDonough,Shay S. Bidani,Hrishikesh S. Kulkarni,Elizabeth P. Newberry,Keely G. McDonald,Rodney D. Newberry
标识
DOI:10.1080/19490976.2023.2284240
摘要
Obesity and the metabolic syndrome are complex disorders resulting from multiple factors including genetics, diet, activity, inflammation, and gut microbes. Animal studies have identified roles for each of these, however the contribution(s) specifically attributed to the gut microbiota remain unclear, as studies have used combinations of genetically altered mice, high fat diet, and/or colonization of germ-free mice, which have an underdeveloped immune system. We investigated the role(s) of the gut microbiota driving obesity and inflammation independent of manipulations in diet and genetics in mice with fully developed immune systems. We demonstrate that the human obese gut microbiota alone was sufficient to drive weight gain, systemic, adipose tissue, and intestinal inflammation, but did not promote intestinal barrier leak. The obese microbiota induced gene expression promoting caloric uptake/harvest but was less effective at inducing genes associated with mucosal immune responses. Thus, the obese gut microbiota is sufficient to induce weight gain and inflammation.
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