Figure 5.

Mechanisms of dietary fiber in the gut. Dietary fibers are carbohydrate polysaccharides; not hydrolyzed by digestive enzymes in gastrointestinal tract and are associated with a low risk for CVD. (A) Dietary fibers elevate the fecal excretion of bile acid, decrease its re-uptake in the small intestine, and inhibit bile acid permeation. A reduced enterohepatic pool of bile acid stimulates the CYP7A (the rate-limiting enzyme involved in the production of bile acid), which, in turn, enhances liver uptake of LDL-C from blood through the upregulation of LDL-R and HMGCR. (B,C) Dietary fibers exhibit fewer calories and their consumption results in a prolonged digestion time with delayed gastric emptying. Additionally, it leads to an increase in bulk-forming and satiety, as well as viscosity-induced reduced absorption of cholesterol, which eventually lower the concentration of LDL-C. (D) Reduced cholesterol synthesis from SCFAs, produced by dietary fibers fermentation in the intestine, contributes to decrease the concentration of LDL-C. Certain SCFAs (propionate) enhances the release of PYY and GLP-1, both of which contribute to reduce LDL-C concentration. Additionally, dietary fibers intake leads to reduced fat uptake, altering the production of adipokines (TNF-α, resistin, and leptin), which play key roles in lipid metabolism and improving cholesterol concentration. The viscosity of dietary fibers reduces the intestinal absorption of glucose, leading to decreased secretion of insulin. Insulin is responsible for stimulating HMGCR; thus, lower insulin could decrease the concentration of LDL-C.