Dietary beta-glucans lower the blood concentrations of cholesterol in animals and humans. Recent studies have uncovered mechanisms by which dietary beta-glucans may regulate cholesterol homeostasis. There is evidence that beta-glucans sequester bile acids in the intestine, reducing their
reabsorption and return to the liver. Reducing hepatic bile acid concentrations activates the enzyme
CYP7A1, which converts cholesterol into bile acids. This action leads to a reduction of hepatic cell
cholesterol content, which up-regulates low-density lipoprotein (LDL) receptor synthesis and thereby
accelerates the transportation of LDL-cholesterol from the blood into hepatocytes. Reduced intracellular
cholesterol also up-regulates the hepatic synthesis of 3-hydroxy-3-methylglutaryl coenzyme A reductase,
the rate-limiting enzyme in cholesterol synthesis. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase and could therefore provide an additive effect in suppressing hepatocyte cholesterol to that produced by enhancing its depletion with beta-glucans. Through this combination of agents, one would expect a greater clearance of LDL from the plasma with lower steady state levels of LDL-cholesterol.