Dietary lipids, gut microbiota and lipid metabolism

Abstract

The gut microbiota is a central regulator of host metabolism. The composition and function of the gut microbiota is dynamic and affected by diet properties such as the amount and composition of lipids. Hence, dietary lipids may influence host physiology through interaction with the gut microbiota. Lipids affect the gut microbiota both as substrates for bacterial metabolic processes, and by inhibiting bacterial growth by toxic influence. The gut microbiota has been shown to affect lipid metabolism and lipid levels in blood and tissues, both in mice and humans. Furthermore, diseases linked to dyslipidemia, such as non-alcoholic liver disease and atherosclerosis, are associated with changes in gut microbiota profile. The influence of the gut microbiota on host lipid metabolism may be mediated through metabolites produced by the gut microbiota such as short-chain fatty acids, secondary bile acids and trimethylamine and by pro-inflammatory bacterially derived factors such as lipopolysaccharide. Here we will review the association between gut microbiota, dietary lipids and lipid metabolism.

Keywords: Atherosclerosis; Bile acid; Diet; Dietary lipid; Dysbiosis; Dyslipidemia; FXR; Fatty acid; Gut microbiota; Gut permeability; Inflammation; LPS; Lipid; Lipid metabolism; Lipopolysaccharides; Microbiome; NAFLD; Non-alcoholic liver disease; TGR5; TMA; TMAO; Trimethylamine N-oxide.

Fig. 1

Interaction between dietary lipids and the gut microbiota influences host physiology. Free fatty acids are produced from lipid precursors by the action of lipases. Fatty acids may have antibacterial activity or may be utilized as metabolic substrates by gut bacteria, thereby affecting gut microbiota profile and production of microbial metabolites. This may influence host physiology and health

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