Gut microbiota induces weight gain and inflammation in the gut

Obesity and the metabolic syndrome are complex disorders resulting from multiple factors including genetics, diet, physical activity, inflammation, and gut microbes. Animal studies have identified roles for each of these, however surprisingly 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. In this study, we show, for the first time, that human fecal gut microbes promote obesity and inflammation in mice with a fully developed immune system, independent of manipulations of genetics and diet. We find that the obese human microbiota alone is sufficient to cause weight gain and systemic and local inflammation in the gut and adipose tissue and contrary to studies of gut microbes using animals on obesogenic diets, these changes occur in absence of gut barrier leak.

肥胖与代谢综合征（metabolic syndrome）是一类由遗传、膳食、体力活动、炎症反应及肠道菌群（gut microbiota）等多种因素共同介导的复杂疾病。既往动物研究已证实上述各类因素的致病作用，但令人意外的是，肠道菌群的特异性贡献仍未明确——既往相关实验多采用基因工程改造小鼠、高脂膳食（high fat diet）模型，或使用免疫系统发育不全的无菌小鼠（germ free mice）进行菌群定植。本研究首次证实，人类粪便源肠道微生物可在免疫系统发育完全的小鼠体内诱导肥胖与炎症反应，且该效应不受遗传与膳食干预的影响。研究发现，仅依靠肥胖人群的肠道菌群即可引发小鼠体重增加，以及肠道与脂肪组织的全身性与局部炎症反应；与此前采用致肥胖膳食（obesogenic diets）饲养动物开展的肠道菌群研究不同，本研究中的相关变化并未伴随肠道屏障渗漏（gut barrier leak）现象。