Transintestinal cholesterol excretion: A secondary, nonbiliary pathway contributing to reverse cholesterol transport.

Transintestinal cholesterol excretion: A secondary, nonbiliary pathway contributing to reverse cholesterol transport.
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DOI:
10.1002/hep.29341
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发表时间:
2017-10
期刊:
Hepatology (Baltimore, Md.)
影响因子:
--
通讯作者:
Tso P
Tso P
中科院分区:
其他
文献类型:
--
作者:
Wang DQ;Portincasa P;Tso P

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Cholesterol is an important component of cellular membranes. However, when excess cholesterol is accumulated within the cell, it becomes cytotoxic. Because almost all cells in the major tissues need a continuous supply of cholesterol, a complex series of biosynthetic, transport, and regulatory mechanisms have evolved in the body. Cholesterol can be obtained from the intestinal absorption derived from diet and bile as well as the de novo biosynthesis from acetyl coenzyme A within the body. Because human cells do not possess enzymes to degrade the ring structure of cholesterol, this sterol cannot be metabolized to CO2 and water. Thus, excess cholesterol must be excreted to prevent a potentially hazardous accumulation in the body. To achieve this task, cholesterol is usually excreted from the body either as an unaltered molecule or after conversion to other sterol products such as bile acids and steroid hormones. Consequently, there is little net accumulation of cholesterol in the body, and yet sufficient cholesterol is always available to meet the metabolic needs of the various tissues.Classically, the reverse cholesterol transport (RCT) encompasses the transporting of excess cholesterol accumulating within peripheral tissues back to the liver for biliary excretion into the feces (Fig. 1). In the late 1950s, a novel nonbiliary transport route for RCT was proposed,(1) challenging this classic view of RCT by demonstrating that the intestine also significantly contributes to mass fecal neutral sterol (FNS) excretion,
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