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Increased plasma HDL cholesterol levels and biliary cholesterol excretion in hamster by LCAT overexpression
Author(s) -
Zhang Ai-Hong,
Gao Song,
Fan Jiang-lin,
Huang Wei,
Zhao Tie-Qiang,
Liu George
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.06.017
Subject(s) - hamster , reverse cholesterol transport , cholesterol , sterol o acyltransferase , endocrinology , medicine , lecithin , lecithin—cholesterol acyltransferase , cholesterol 7 alpha hydroxylase , high density lipoprotein , chemistry , bile acid , lipoprotein , enzyme , biology , biochemistry
Lecithin cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of high density lipoprotein (HDL), which has been found inversely correlated with atherosclerosis. Adenovirus mediated overexpression of human LCAT (hLCAT) in hamsters resulted in increased levels of plasma total cholesterol, HDL cholesterol, phospholipids and enlarged particle size of HDL. It also increased cholesterol and total bile acid concentrations in bile. Hepatic mRNA level of cholesterol 7α‐hydroxylase increased 2.7‐fold in hamsters. However, such effects were not observed in mice in a parallel experiment. This study suggests that overexpression of hLCAT in hamsters facilitated reverse cholesterol transport. Similar metabolic changes in humans might modify atherogenic risk.