Debugging Metabolic Disease

Science Signaling  13 Apr 2010:
Vol. 3, Issue 117, pp. ec109
DOI: 10.1126/scisignal.3117ec109

Obesity, now officially recognized as an epidemic in many developed nations, is a key component of “metabolic syndrome,” an array of metabolic disturbances that increase an individual’s risk of developing diabetes and heart disease. The rise in obesity rates has been largely attributed to the growing imbalance between food intake and energy expenditure, but recent provocative work has suggested a possible link between obesity and the composition of microbes residing within the gut. Vijay-Kumar et al. (see the Perspective by Sandoval and Seeley) now find that mutant mice deficient in a component of the innate immune system (which defends the body against microbial pathogens) develop hallmark features of metabolic syndrome, accompanied by changes in gut microbiota. Notably, transfer of gut microbiota from the mutant mice to wild-type mice conferred several features of metabolic syndrome to the recipients. Thus, the development of metabolic syndrome may indeed be influenced by gut microbes that are regulated by the innate immune system.

M. Vijay-Kumar, J. D. Aitken, F. A. Carvalho, T. C. Cullender, S. Mwangi, S. Srinivasan, S. V. Sitaraman, R. Knight, R. E. Ley, A. T. Gewirtz, Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5. Science 328, 228–231 (2010). [Abstract] [Full Text]

D. A. Sandoval, R. J. Seeley, The microbes made me eat it. Science 328, 179–180 (2010). [Summary] [Full Text]