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. 2019 Dec 17;8(12):2227. doi: 10.3390/jcm8122227

Figure 1.

Figure 1

Mechanisms of the role of microbiota in host lipoprotein metabolism. The intestine and liver are two major organs involved in lipid and lipoprotein metabolism. In the intestine, BA emulsify fat into smaller fat particles which allows lipases to breakdown triglycerides into fatty acids. Fatty acids can then be absorbed and be used as substrates for CM assembly. CM production contributes to postprandial TG levels. Microbiota within intestine generates SCFA, secondary BA and LPS. SCFA and FA can activate receptors on enteroendocrine L-cells to release GLP-1/GLP-2 which regulate postprandial CM production. SCFA and BA are absorbed and enter the portal circulation. In the liver, SCFA can act as substrates for de novo lipogenesis and contribute to VLDL production. BA can activate FXR and TGR5 signaling pathways to regulate VLDL assembly. VLDL and its products IDL and LDL contribute to fasting TG levels. BA, bile acids; CM, chylomicron; FXR, farnesoid X receptor; FA, fatty acids; GLP-1/2, Glucagon-like peptide 1/2; IDL, intermediate density lipoprotein; LPS, lipopolysaccharide; LDL, low density lipoprotein; SCFA, short-chain fatty acid; TGR5, G-protein-coupled bile acid receptor; TG, triglyceride; VLDL, very low density lipoproteins.