最新的一项研究表明，肥胖及胰岛素抵抗等代谢性疾病也是可传染的，通过小鼠的实验已证实：通过可以传播肠道细菌可使得小鼠改变食欲及代谢状态。
传统观点认为，久坐的工作生活习惯加之高卡路里食物的过量摄入是造成肥胖的主要原因，简言之即“好吃懒做”。但美国Emory University的Matam Vijay-Kumar和Gewirtz等人在前人研究的基础上，意外的发现TLR5（Toll样受体-5）缺陷的小鼠较正常小鼠重20%，而且血甘油三酯、血胆固醇、血压及血糖偏高。TLR5缺陷的小鼠比正常小鼠进食多10%，经限制饮食后前者体重下降，但同时对胰岛素的反应下降（即胰岛素抵抗）；在经高脂饮食后前者体重快速增加并表现出“糖尿病”和“代谢综合征”表现。
TLR5已被证实在肠道细菌防御上起重要作用，TLR5缺陷的小鼠更易患炎症性肠病、结肠炎等。使用强力的抗生素杀灭大部分肠道细菌后，TLR5缺陷小鼠的“代谢综合征”症状好转。更重要的事，将TLR5缺陷小鼠的肠道细菌转移到正常小鼠，正常小鼠也表现出“代谢综合征”症状。
Gewirtz等人表示，他们将进一步研究TLR5缺陷小鼠肠道细菌的差异及这些差异如何影响其代谢，并最终阐明TLR5基因在人体上的作用。（生物谷Bioon.com）
生物谷推荐原文出处：
Science 10.1126/science.1179721
Metabolic Syndrome and Altered Gut Microbiota in Mice Lacking Toll-Like Receptor 5
Matam Vijay-Kumar, Jesse D. Aitken, Frederic A. Carvalho, Tyler C. Cullender, Simon Mwangi, Shanthi Srinivasan, Shanthi V. Sitaraman, Rob Knight, Ruth E. Ley, Andrew T. Gewirtz
Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota and, importantly, transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.
