Intestinal bacteria contribute to changes in appetite and metabolism/Implications for Metabolic Syndrome
Bacteria that helps digest food can cause obesity if the bacteria becomes unregulated and certain bacteria overpopulate and cause a low-leval inflammation that leads to a pre-diabetic condition and elevated appetite.
Scientist discovered 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 (excessive appetite) and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity.
The metabolic changes correlated with changes in the composition of the bacteria present in the gut. Also transfer of the gut bacteria from TLR5-deficient mice to wild-type germ-free mice caused many features of metabolic syndrome to the germ-free mice.
Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice.
The scientists concluded that the results support the emerging view that the gut microbiota (composition of bacteria in the intestines) contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.
SOURCE: Vijay-Kumar M, Aitken JD, Carvalho FA, Cullender TC, Mwangi S, Srinivasan S, Sitaraman SV, Knight R, Ley RE, Gewirtz AT. Metabolic Syndrome and Altered Gut Microbiota in Mice Lacking Toll-Like Receptor 5. Science. 2010 Mar 4.
See also …
Wikipedia: Metabolic Syndrome
