Date of this Version
Genome Biology 2009, 10:203; doi:10.1186/gb-2009-10-1-203
Modulation of host signaling by the products of microbial activity in the gut may affect weight gain and fat formation.
The relationship between humans and the population of indigenous microorganisms in their intestines (the gut microbiota) is ancient and important. In a recent survey exploring the relationship between mammals and their microbiota it was found that individuals of the same species were more likely to have a similar gut microbiota than mammals of different species . This observation held true regardless of the geographic separation between the two hosts. These results indicate that the composition of the microbiota is dependent more on the identity of the host than on geography and that host and microbiota have coevolved for their mutual benefit . In essence, we are a mosaic of millions of bacterial genomes that work in concert with the one human genome.
The bulk of our bacterial colleagues are located in the gastrointestinal tract, where the density of bacterial cells in the colon has been estimated at 1011-1012 cells/ml . This close association is mutualistic in nature. The bacteria gain a nutrient-rich environment and humans gain a vast genetic repertoire of encoded physiological functions. Within this repertoire are many genes whose products may help humans adapt to changes in diet and lifestyle. With their short generation times and abilities to swap DNA, the bacteria in our gut adapt and evolve to meet the demands of their everchanging world, and because their world is our world they serve to complement the human genome. The interactions between host and microbiota determine the success of this relationship. In a recent study published in the Proceedings of the National Academy of Sciences, Samuel and colleagues  demonstrate that short-chain fatty acids (SCFAs) produced by the microbiota signal through the host G-protein-coupled receptor (GPCR) Gpr41 and influence weight gain and adiposity.