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The "Dietary fiber-mediated cholesterol reduction pathway" refers to the collection of physiological processes through which soluble dietary fibers lower blood cholesterol levels. This is not a single molecular target but an integrated set of mechanisms involving: • **Binding and sequestration**: Soluble fibers such as β-glucan, pectin, guar gum, psyllium form viscous gels in the small intestine that bind bile acids—compounds synthesized from hepatic cholesterol—and prevent their reabsorption. This increases fecal excretion of bile acids. To compensate for lost bile acids, the liver converts more circulating cholesterol into new bile acids, thereby reducing plasma LDL-cholesterol concentrations[1][2][3][4][6]. • **Reduced absorption**: The gel-forming property also slows intestinal transit time and reduces absorption efficiency for both dietary fat/cholesterol and reabsorbed biliary lipids[1][2]. • **Microbial fermentation**: In the colon, certain soluble fibers are fermented by gut bacteria into short-chain fatty acids like propionate. Propionate can inhibit HMG-CoA reductase—the rate-limiting enzyme in endogenous hepatic cholesterol synthesis—further lowering blood lipid levels[1]. • **Gut microbiome effects**: Dietary fiber promotes growth of beneficial bacteria such as Lactobacillus and Bifidobacterium species that possess enzymes capable of deconjugating bile salts. This enhances their excretion rather than recycling back to the liver[1]. These combined actions result in modest but clinically significant reductions in total serum cholesterol and LDL-C without affecting HDL-C or triglycerides significantly when adequate amounts (~5–10 g/day) are consumed regularly through foods like oats, legumes, fruits/vegetables rich in soluble fiber[4][5]. Because this entry describes an entire *physiological process* rather than a discrete druggable molecule or receptor classically considered therapeutic targets (e.g., enzyme/receptor/transporter), it should be flagged as incorrect for structured drug-target databases. If you need information on specific molecules within this pathway—such as HMG-CoA reductase or particular types/species involved—please specify further.
• Increased excretion of bile acids by binding them in the intestine • Reduced absorption of dietary cholesterol due to increased intestinal viscosity • Modulation of gut microbiota leading to increased deconjugation and excretion of bile acids • Production of short-chain fatty acids from fermentation by gut bacteria that suppress hepatic cholesterol synthesis via inhibition of HMG-CoA reductase
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