最新的一項(xiàng)研究表明,，肥胖及胰島素抵抗等代謝性疾病也是可傳染的,，通過小鼠的實(shí)驗(yàn)已證實(shí)：通過可以傳播腸道細(xì)菌可使得小鼠改變食欲及代謝狀態(tài),。
傳統(tǒng)觀點(diǎn)認(rèn)為,，久坐的工作生活習(xí)慣加之高卡路里食物的過量攝入是造成肥胖的主要原因,，簡(jiǎn)言之即“好吃懶做”,。但美國Emory University的Matam Vijay-Kumar和Gewirtz等人在前人研究的基礎(chǔ)上,，意外的發(fā)現(xiàn)TLR5（Toll樣受體-5）缺陷的小鼠較正常小鼠重20%，而且血甘油三酯、血膽固醇,、血壓及血糖偏高,。TLR5缺陷的小鼠比正常小鼠進(jìn)食多10%，經(jīng)限制飲食后前者體重下降,，但同時(shí)對(duì)胰島素的反應(yīng)下降（即胰島素抵抗）,；在經(jīng)高脂飲食后前者體重快速增加并表現(xiàn)出“糖尿病”和“代謝綜合征”表現(xiàn)。
TLR5已被證實(shí)在腸道細(xì)菌防御上起重要作用,，TLR5缺陷的小鼠更易患炎癥性腸病,、結(jié)腸炎等。使用強(qiáng)力的抗生素殺滅大部分腸道細(xì)菌后,，TLR5缺陷小鼠的“代謝綜合征”癥狀好轉(zhuǎn),。更重要的事，將TLR5缺陷小鼠的腸道細(xì)菌轉(zhuǎn)移到正常小鼠,，正常小鼠也表現(xiàn)出“代謝綜合征”癥狀,。
Gewirtz等人表示，他們將進(jìn)一步研究TLR5缺陷小鼠腸道細(xì)菌的差異及這些差異如何影響其代謝,，并最終闡明TLR5基因在人體上的作用,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
