Gut microbiota-host interactions. The short-chain fatty acids (SCFA) propionate, acetate and butyrate produced by bacterial fermentation of indigestible polysaccharides trigger the release of the satietogenic gut hormones GLP-1 and PYY from enteroendocrine L-cells; these hormones in turn regulate ingestive behavior by acting on the hypothalamus. Release of gastric inhibitory polypeptide (GIP) from enteroendocrine K-cells triggered by butyrate is a potent promoter of glucose-dependent insulin secretion, acting in concert with GLP-1. Through direct trophic effects on the intestinal epithelium and by triggering the release of GLP-2 from L-cells, butyrate makes the epithelial barrier less permeable through increased mucus production and tight junction expression. L-carnitine and phosphatidylcholine, both constituents of red meat, are metabolized by intestinal bacteria, releasing trimethylamine (TMA). Following absorption to the portal circulation, TMA is converted by hepatic flavin-containing monooxygenase to the atherogenic trimethylamine-N-oxide (TMAO). The gut microbiota is heavily involved in bile acid metabolism by performing deconjugation and dehydroxylation. Cholic acid lowers hepatic lipogenesis by acting on the farnesoid X receptor and increases the energy expenditure through fat oxidation by inducing the enzymatic conversion of inactive thyroxine to the active tri-iodothyronine in brown adipose tissue (BAT) and skeletal muscle. Abbreviations: CNS, central nervous system.