Fig. 2.

Mechanisms linking the gut microbiota to lipid metabolism and pathophysiological conditions associated with dyslipidemia. Short-chain fatty acids regulate host lipid metabolism by supplying the host with energy, improving peripheral tissue metabolism and stimulating incretin hormone production. The gut microbiota transforms choline and L-carnitine to trimethylamine (TMA). TMA is transformed into trimethylamine N-oxide (TMAO) that may promote increased atherosclerosis through mechanisms related to lipid metabolism and inflammation. Bile acids regulate metabolism by binding to farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (TGR5) in several different tissues. Deconjugation of bile acids reduces absorption and increase excretion of bile acids. Increased gut permeability facilitates translocation of lipopolysaccharide (LPS) over the intestinal epithelium. LPS induce inflammation through TLR4 that may result in metabolic perturbations and contribute to development of metabolic diseases. HDL may neutralize the toxic effect of LPS. PPARγ, peroxisome proliferator-activated receptor gamma; GPR43, G-protein coupled receptors GPR43(FFAR2); GPR41, G-protein coupled receptors GPR43(FFAR3); SCFA, short-chain fatty acid; PYY, peptide YY; TLR4, toll-like receptor 4