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Niemann-Pick C1-Like 1 (NPC1L1) Protein in Intestinal and Hepatic Cholesterol Transport

Jia, Lin, Betters, Jenna L., Yu, Liqing·2011·Annual Review of Physiology
DOI 10.1146/annurev-physiol-012110-142233PMC PMC3965667
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Abstract

Increased blood cholesterol is an independent risk factor for atherosclerotic cardiovascular disease. Cholesterol homeostasis in the body is controlled mainly by endogenous synthesis, intestinal absorption, and hepatic excretion. Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein localized at the apical membrane of enterocytes and the canalicular membrane of hepatocytes. It functions as a sterol transporter to mediate intestinal cholesterol absorption and counterbalances hepatobiliary cholesterol excretion. NPC1L1 is the molecular target of ezetimibe, a potent cholesterol absorption inhibitor that is widely used in treating hypercholesterolemia. Recent findings suggest that NPC1L1 deficiency or ezetimibe treatment also prevents diet-induced hepatic steatosis and obesity in addition to reducing blood cholesterol. Future studies should focus on molecular mechanisms underlying NPC1L1-dependent cholesterol transport and elucidation of how a cholesterol transporter modulates the pathogenesis of metabolic diseases.

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  • Statins and NPC1L1 inhibitors enhance LDLR expression in hepatocytes, thereby promoting serum LDL-C clearance.

    “Besides PCSK9 antibodies, current clinical therapies including statins13,14 and NPC1L1 (NPC1 like intracellular cholesterol transporter 1) inhibitors15enhance LDLR expression in hepatocytes, thereby promoting serum LDL-C clearance.”

    From ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver (2025) · cites this paper as [15]

    The Introduction says ezetimibe inhibits intestinal cholesterol absorption and lowers blood LDL-C. The section on genetic variation in NPC1L1 says increased absorption downregulates hepatic LDL receptors and reduces LDL clearance. These passages support the proposed pathway, but do not directly establish that NPC1L1 inhibitors enhance LDLR expression in hepatocytes or that this increase causes their LDL-C-lowering effect. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

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Metadata

Authors
Jia, L., Betters, J. L., & Yu, L.
Venue
Annual Review of Physiology
Publisher
Annual Reviews
Published
2011-03-17
Volume
73
Issue
1
Pages
239-259
ISSN
  • 0066-4278
  • 1545-1585
DOI
10.1146/annurev-physiol-012110-142233
PMC
PMC3965667
Cited by
356
References
6
Language
en

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