1978
DOI: 10.3109/00365517809104930
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Plasma Lecithin:Cholesterol Acyltransferase Activity and the Lipoprotein Abnormalities of Liver Disease

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1983
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Cited by 16 publications
(4 citation statements)
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“…In addition, APOA1 and APOA2 are the main components of high-density lipoprotein, while APOB is the main component of low-density lipoproteins (LDLs) and very low-density lipoproteins. LCAT converts free cholesterol in serum into cholesterol esters that can be stored in high-density lipoprotein and then transported to the liver for further metabolism ( 58 ). APOB is the recognition site of the LDL receptor on the plasma membrane, and a functional study using human HepG2 cells showed that enhanced cholesterol metabolism in hepatocytes stimulates the secretion of APOB and reduces the uptake of LDL ( 59 ).…”
Section: Discussionmentioning
confidence: 99%
“…In addition, APOA1 and APOA2 are the main components of high-density lipoprotein, while APOB is the main component of low-density lipoproteins (LDLs) and very low-density lipoproteins. LCAT converts free cholesterol in serum into cholesterol esters that can be stored in high-density lipoprotein and then transported to the liver for further metabolism ( 58 ). APOB is the recognition site of the LDL receptor on the plasma membrane, and a functional study using human HepG2 cells showed that enhanced cholesterol metabolism in hepatocytes stimulates the secretion of APOB and reduces the uptake of LDL ( 59 ).…”
Section: Discussionmentioning
confidence: 99%
“…On the other hand, there is no clear-cut correlation between plasma vitamin E and the various serum lipid fractions; this finding is not in acc ordance with previous reports on hyperlipemic patients (10) and control subjects (11,12). Thi s ma y be due to the fact that the intraintestin al bile salt deficiency and the re sulting poor vitamin E ab sorption are independent of the mechanism s responsible for the lipid disorders in chol estatic patients (13).…”
Section: Discussioncontrasting
confidence: 69%
“…While enzyme activities were not measured in this study, it is likely that reductions in LCAT activity contribute to the development of LP-Z. Previous studies support the hypothesis that LCAT, CETP, HL, apoA-I and apoA-IV are reduced in patients with liver disease and cirrhosis [ 7 , 15 , 26 , 27 , 29 ]. Typical of patients with liver diseases, the high bilirubin samples exhibited low HDL-C and HDL particles.…”
Section: Discussionmentioning
confidence: 69%
“…These lipid changes may be explained by differences in the levels and activities of key proteins that regulate lipoprotein metabolism in subjects with liver disease. For example, patients with severe liver disease have lower circulating LCAT, cholesteryl ester transfer protein (CETP) and higher HL than healthy subjects [ 15 , 25 , 27 ], raising the possibility that defective lipoprotein remodeling and catabolism may account for the appearance of LP-Z. This is in contrast to elevated LCAT activity in subjects with non-alcoholic fatty liver disease (NAFLD), normal bilirubin levels and mildly elevated liver enzymes [ 28 ].…”
Section: Discussionmentioning
confidence: 99%