Journal
ANNUAL REVIEW OF PHYSIOLOGY, VOL 73
Volume 73, Issue -, Pages 239-259Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-012110-142233
Keywords
ezetimibe; fat absorption; hepatic steatosis; obesity
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Funding
- NIDDK NIH HHS [F32 DK084582, R01 DK085176, 1F32DK084582-01, R01DK085176] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [F32DK084582, R01DK085176] Funding Source: NIH RePORTER
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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 I 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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