Intestinal bacteria drive obesity and metabolic disease in immune-altered mice

"Mice lacking a gene called TLR5 have an altered ability to recognize and control bacteria in their intestines, leading them to develop obesity and insulin resistance, which is often referred to as "pre-diabetes." The bacteria appear to influence appetite and metabolism rather than how well calories are absorbed. Obesity and insulin resistance can be transferred from TLR5-deficient mice via intestinal bacteria."
Intestinal bacteria drive obesity and metabolic disease in immune-altered mice

Notes:

• GSK-3b regulates TLR production including TLR5. Studies have demonstrated that TLR signaling increases IL-10 which has an anti-inflammatory effect and inhibition of GSK-3b may be protective against endotoxic shock.
• Changes in inflammatory cytokines may influence TLR functioning in mesenchymal stromal cells.

Martin, M., Rehani, K., Jope, R. S., and Michalek, S. M. (2005). Toll-like receptor-mediated cytokine production is differentially regulated by glycogen synthase kinase 3. Nature immunology, 6(8):777-784. http://www.citeulike.org/user/HEIRS/article/260512
Abreu, M. T. (2010). Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function. Nature Reviews Immunology, 10(2):131-144. http://www.citeulike.org/user/HEIRS/article/6589668
Palmer, Eric. Innate immune defense against intestinal bacteria. Videocast. National Institutes of Health. Retrieved on Monday March 1, 2010. http://videocast.nih.gov/ram/iig102109.ram