The absorption of fat in the small intestine is dependent on the availability of bile acids from biliary secretions which also contain free cholesterol. Both bile acids (>95%) and biliary cholesterol are salvaged by an energy-dependent process in the terminal ileum. This active process of reabsorption via the enterohepatic circulation is tightly controlled by a feedback mechanism that is sensitive to hepatic levels of cholesterol. Thus, the reabsorption of cholesterol downregulates the activity of 7-α-hydroxylase in the liver, shutting down the further production of bile acids. Substances in the lumen of the gut that are capable of binding or competing with bound bile acids, such as naturally occurring plant sterols or soluble nonstarch polysaccharides (NSPs), prevent their reabsorption which, in effect, interrupts the enterohepatic circulation. This depletes the supply of cholesterol and accelerates the production of bile acids, depleting the liver of cholesterol (Figure 6.6). To replenish this loss, liver cells respond by increasing their uptake of cholesterol from circulating lipopro-teins in the blood, with the result of a decrease in blood cholesterol. Interruption of the enterohepatic circulation helps to explain the cholesterol-lowering action of some of the earliest known cholesterol-low-ering drugs, but also such dietary constituents as the phytosterols (sitosterol and stanol esters) and soluble fiber or NSPs.
Figure 6.6 Interruption of the entero-hepatic circulation. LDL, low-density lipoprotein;HMG-CoA,3-hydroxy-3-methyl-glutaryl-coenzyme A.
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