The bacterial population of the intestine also plays an important role in dietary lipid uptake and metabolism. Fermentation by the gut microbiota allows host animals to utilize dietary plant polysaccharides that would otherwise be indigestible by converting them to metabolizable short-chain fatty acids and monosaccharides (60). Multiple studies over the last decade have shown effects of changes in composition of the gut microbiota on adiposity, serum lipids, and tissue lipids in mammals (61–66). However, determining mechanisms by which bacteria may cause global changes in vertebrate host physiology has been difficult as the composition of the gut microbiota also changes in response to changes in diet (67, 68). The larval zebrafish model was recently used to investigate aspects of the relationship between gut bacteria and lipids involving processes other than short-chain fatty acid synthesis: when larvae raised germ-free were given a high-fat meal labeled with fluorescent fatty acids, less fluorescence accumulated in the intestinal epithelium when compared with conventionally raised larvae, showing that at least some members of the microbiota are necessary to promote uptake of dietary lipids. Monoassociated larvae (larvae raised germ-free and then inoculated with a single bacterial species) colonized with the Firmicutes strain Exiguobacterium sp. were used to demonstrate that this bacterial strain alone was sufficient to promote intestinal fatty acid uptake to a point where fluorescence could be observed in extra-intestinal tissues. Furthermore, experiments using conditioned media from this strain and two others also revealed significant increases in enterocyte lipid droplet number over untreated germ-free larvae, suggesting that a factor secreted by these species is involved in promoting dietary lipid uptake (69). The exact mechanism for this host–microbe relationship is currently uncharacterized, as is the evolutionary advantage of promoting host lipid uptake for these microbial species.