ISME J：阴沟肠杆菌可能是肥胖的关键原因

　　“人要是发胖，哪怕喝凉水都会长肉。”不少减肥的人士会有这种感慨。究竟什么导致肥胖？近来上海交大教授发表的一篇学术成果显示，一种叫做阴沟肠杆菌的肠道细菌是造成肥胖的直接元凶之一。这也是国际上首次证明肠道细菌与肥胖之间具有直接因果关系。

　　这一成果是上海交大赵立平教授领导的实验室实验证明的，并发表在12月13日出版的国际微生物生态学领域的顶级学术期刊ISME Journal上。

　　在实验中，一种来自肥胖病人的肠道细菌阴沟肠杆菌在无菌小鼠内引起了严重的肥胖和胰岛素抵抗，这为肠道菌群参与人体肥胖、糖尿病发生、发展的“慢性病的肠源性学说”提供了最直接的实验证据。

　　赵立平介绍说，他负责的实验室找到的阴沟肠杆菌可以产生内毒素，能够让本来吃高脂饲料吃不胖的无菌小鼠发展出严重的肥胖症，同时能够引起小鼠炎症和胰岛素抵抗，也可以关闭消耗脂肪需要的基因、激活合成脂肪的基因，是国际上一直在寻找的能引起肥胖的细菌。

　　科研人员在临床研究中发现，一种可以产生内毒素的致病菌——阴沟肠杆菌在一个体重达175公斤的肥胖患者肠道里过度生长，占到总菌量的三分之一之多。经过用一种特殊设计的营养配方干预以后，这种病菌数量很快下降到检测不出来的水平。而患者的体重在将近半年里下降了51.4公斤，高血糖、高血压和高血脂等症状也恢复正常。

　　人体肠道里生活着大约1000种细菌，统称为肠道菌群，其总重量大约有1.5千克，其细胞总数量是人体自身细胞总数的10倍。

与肥胖相关的拓展阅读：

• 上海交大教授发现肥胖细菌
• RSNA:腹型肥胖男子骨质疏松风险增加
• ACCOMPLISH:并非所有肥胖高血压患者需使用利尿剂
• Cancer Res：肥胖患者有较高的癌症发病率和较差的预后
• Eur Heart J：“肥胖悖论”：肥胖患者卒中后预后更佳？
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Lipopolysaccharide endotoxin is the only known bacterial product which, when subcutaneously infused into mice in its purified form, can induce obesity and insulin resistance via an inflammation-mediated pathway. Here we show that one endotoxin-producing bacterium isolated from a morbidly obese human’s gut induced obesity and insulin resistance in germfree mice. The endotoxin-producing Enterobacter decreased in relative abundance from 35% of the volunteer’s gut bacteria to non-detectable, during which time the volunteer lost 51.4kg of 174.8kg initial weight and recovered from hyperglycemia and hypertension after 23 weeks on a diet of whole grains, traditional Chinese medicinal foods and prebiotics. A decreased abundance of endotoxin biosynthetic genes in the gut of the volunteer was correlated with a decreased circulating endotoxin load and alleviated inflammation. Mono-association of germfree C57BL/6J mice with strain Enterobacter cloacae B29 isolated from the volunteer’s gut induced fully developed obesity and insulin resistance on a high-fat diet but not on normal chow diet, whereas the germfree control mice on a high-fat diet did not exhibit the same disease phenotypes. The Enterobacter-induced obese mice showed increased serum endotoxin load and aggravated inflammatory conditions. The obesity-inducing capacity of this human-derived endotoxin producer in gnotobiotic mice suggests that it may causatively contribute to the development of obesity in its human host.