TY - JOUR
T1 - Metabolie syndrome and altered gut microbiota in mice lacking toll-like receptor 5
AU - Vijay-Kumar, Matam
AU - Aitken, Jesse D.
AU - Carvalho, Frederic A.
AU - Cullender, Tyler C.
AU - Mwangi, Simon
AU - Srinivasan, Shanthi
AU - Sitaraman, Shanthi V.
AU - Knight, Rob
AU - Ley, Ruth E.
AU - Gewirtz, Andrew T.
PY - 2010/4/9
Y1 - 2010/4/9
N2 - Metabolie syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Mere, 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 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.
AB - Metabolie syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Mere, 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 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.
UR - http://www.scopus.com/inward/record.url?scp=77950250064&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77950250064&partnerID=8YFLogxK
U2 - 10.1126/science.1179721
DO - 10.1126/science.1179721
M3 - Article
C2 - 20203013
AN - SCOPUS:77950250064
SN - 0036-8075
VL - 328
SP - 228
EP - 231
JO - Science
JF - Science
IS - 5975
ER -