Abstract
Cholesterol is metabolized in the liver by oxidation to bile acids which undergo enterohepatic circulation. In the untreated state, approximately 95 % of the bile acids that are secreted are reabsorbed and returned to the liver, while the small loss is replaced by de novo biosynthesis from cholesterol. Increased excretion of bile acids with the feces increases the rate of oxidation of cholesterol in the liver leading to a partial depletion of the hepatic cholesterol pool. A compensatory increase in uptake via the LDL receptors results in lower serum LDL levels. This can be achieved by addition of a bile acid-binding resin, e.g., cholestyramine, to the food. The binding of unconjugated and conjugated bile-salt anions can be tested in vitro (Johns and Bates 1969).
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References and Further Reading
Cholestyramine Binding
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Boucher, P., Vogel, H.G. (2015). Interruption of Bile Acid Recirculation. In: Hock, F. (eds) Drug Discovery and Evaluation: Pharmacological Assays. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-27728-3_50-1
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DOI: https://doi.org/10.1007/978-3-642-27728-3_50-1
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Publisher Name: Springer, Berlin, Heidelberg
Online ISBN: 978-3-642-27728-3
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