Lecithin-cholesterol acyltransferase and lipid transfer protein activities in liver disease

Tahara, Daigo; Nakanishi, Tomohiro; Akazawa, Shoichi; Yamaguchi, Yoshihiko; Yamamoto, H.; Akashi, M; Chikuba, Nobuhiro; Okuno, Shinichiro; Maeda, Yasuo; Kusumoto, Yukio; Nagataki, Shigenobu

doi:10.1016/0026-0495(93)90166-l

Cited by 37 publications

(20 citation statements)

References 38 publications

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“…[174][175][176] In patients with liver cirrhosis, the withdrawal of alcohol is not sufficient to normalize the low HDL levels. 110 The activity of plasma lectin:cholesteryl acyltransferase (LCAT), an enzyme that esterifies cholesterol in HDL particles, is also decreased with progression of hepatocellular damage, 177 contributing to the low plasma HDL concentration in alcoholic liver disease.…”

Section: Liver Diseasementioning

confidence: 99%

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Effect of Alcohol on Lipids and Lipoproteins in Relation to Atherosclerosis

Hannuksela

Liisanantti

Savolainen

2002

Critical Reviews in Clinical Laboratory Sciences

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Several studies indicate that light-to-moderate alcohol consumption is associated with a low prevalence of coronary heart disease. An increase in high-density lipoprotein (HDL) cholesterol is associated with alcohol intake and appears to account for approximately half of alcohol's cardioprotective effect. In addition to changes in the concentration and composition of lipoproteins, alcohol consumption may alter the activities of plasma proteins and enzymes involved in lipoprotein metabolism: cholesteryl ester transfer protein, phospholipid transfer protein, lecithin:cholesterol acyltransferase, lipoprotein lipase, hepatic lipase, paraoxonase-1 and phospholipases. Alcohol intake also results in modifications of lipoprotein particles: low sialic acid content in apolipoprotein components of lipoprotein particles (e.g., HDL apo E and apo J) and acetaldehyde modification of apolipoproteins. In addition, "abnormal" lipids, phosphatidylethanol, and fatty acid ethyl esters formed in the presence of ethanol are associated with lipoproteins in plasma. The effects of lipoproteins on the vascular wall cells (endothelial cells, smooth muscle cells, and monocyte/macrophages) may be modulated by ethanol and the alterations further enhanced by modified lipids. The present review discusses the effects of alcohol on lipoproteins in cholesterol transport, as well as the novel effects of lipoproteins on vascular wall cells.

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Section: Liver Diseasementioning

confidence: 99%

“…232 The activity of LCAT is reduced in liver steatosis and alcoholic cirrhosis. 177 In subjects without liver disease, LCAT activity has been reported to be unaffected after moderate alcohol intake. 84,220,221 Alcohol consumption with a meal, however, is related to increased LCAT activity.…”

Section: Effect Of Alcohol On Lecithin:cholesterol Acyltransferase Anmentioning

confidence: 99%

Effect of Alcohol on Lipids and Lipoproteins in Relation to Atherosclerosis

Hannuksela

Liisanantti

Savolainen

2002

Critical Reviews in Clinical Laboratory Sciences

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“…This increase corresponded mainly to free cholesterol. A similar situation was found in patients with acute viral hepatitis, which probably reflects the deficiency of lecithin : cholesterol acyltransferase activity characteristic of these diseases (6).…”

Section: Resultsmentioning

confidence: 71%

“…Liver also produces and secretes lecithin : cholesterol acyltransferase 2 ), a plasmatic enzyme that esterifies the cholesterol collected from the cells by HDL (1), and cholesteryl ester transfer protein which allows the exchange of neutral lipids between the different classes of lipoproteins in plasma (2). Liver damage and alterations in the exocrine function of the gland lead to a profound alteration of the plasma lipid profile, modifying the lipoprotein content of total and esterified cholesterol, triacylglycerols, phospholipids (3) and apolipoproteins (4), as well as the activities of lecithin : cholesterol acyltransferase (5), cholesteryl ester transfer protein (6,7) and hepatic lipase ! ) This work was supported in part by the Fondo de Investigaciones Sanitarias (94/0484), Spain.…”

Section: Introductionmentioning

confidence: 99%

Fatty Acid Composition of Lipoprotein Lipids in Hepatobiliary Diseases

Arranz

Lasunción²,

Perales³

et al. 1996

CCLM

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Summary: Liver damage and alterations in the exocrine function of the gland lead to a profound alteration of the plasma lipoprotein profile. To determine whether hepatic disease results in changes in the lipoprotein fatty acid composition, i. e. to determine whether liver function influences the homeostasis of complex lipids in plasma, we studied the fatty acid profile of lipids from VLDL, LDL and HDL, as well as from total plasma, in thirty-one patients of both sexes with hepatobiliary pathology (compensated liver cirrhosis, uncompensated liver cirrhosis, primary biliary cirrhosis, other intrahepatic cholestasis, and acute viral hepatitis). We also studied a group of healthy adults as controls. We present the lipoprotein profile and the fatty acid composition (myristic C14, palmitic C16, palmitoleic C16 : 1, stearic CIS, oleic CIS : 1, linoleic CIS : 2, eicosatrienoic C20 : 3co6 and arachidonic C20 : 4) of lipoprotein and total plasma triacylglycerols, cholesteryl esters and phospholipids. The main observation of this study is that, despite the profound changes in the lipoprotein profile and the lower abundance of polyunsaturated fatty acids in complex lipids, the composition of all triagylglycerols, cholesteryl esters and phospholipids is very similar for the corresponding lipoproteins of patients with hepatobiliary disease and of control subjects. This indicates that in the controls as in the studied patients, the exchange of lipids between plasmatic lipoproteins is very rapid and demonstrates the possible importance of the extrahepatic synthesis of cholesteryl ester transfer protein.

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“…However, remarkably little is currently known about the influence of NAFLD on alterations in circulating LCAT and PLTP activities. Early studies have shown that plasma LCAT activity is impaired in patients with chronic hepatitis, alcoholic liver disease and cirrhosis, coinciding with a decreased plasma cholesterol esterification rate . Another report showed that plasma LCAT mass was unaltered in a small group of only six subjects with hepatic steatosis .…”

Section: Introductionmentioning

confidence: 99%