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Defective glycosylation of cholesteryl ester transfer protein in plasma from alcohol abusers.

https://arctichealth.org/en/permalink/ahliterature9109
Source
Alcohol Alcohol. 2006 Jan-Feb;41(1):18-23
Publication Type
Article
Author
M Johanna Liinamaa
Minna L Hannuksela
Maria E Rämet
Markku J Savolainen
Author Affiliation
Department of Internal Medicine, University of Oulu, PO Box 5000, 90014 Oulu, Finland. johanna.liinamaa@oulu.fi
Source
Alcohol Alcohol. 2006 Jan-Feb;41(1):18-23
Language
English
Publication Type
Article
Abstract
AIMS: Alcohol consumption reduces the carbohydrate content of some glycoproteins, e.g. carbohydrate-deficient transferrin. The aim of this study was to investigate if there is such an alcohol-induced glycosylation defect in plasma cholesteryl ester transfer protein (CETP). A defect in the posttranslational glycosylation of CETP may affect its structure and electrical charge and may therefore affect its function. CETP activity is low in alcohol abusers. METHODS: We studied the effect of alcohol consumption on CETP properties in 10 alcohol abusers and 10 control subjects. CETP was partially purified from lipoprotein-free plasma by FPLC using a Phenyl-Sepharose column. Isoelectric focusing, polyacrylamide gel electrophoresis, and western blotting were performed for partially purified CETP. RESULTS: CETP had a lower molecular weight in the alcohol abusers than in the controls (range 50.6-84.0 kDa in the alcohol abusers vs 51.3-85.0 kDa in the controls). CETP purified from alcohol abusers had a higher isoelectric point, indicating a lower negative charge on the surface of the protein than in the controls' CETP. A similar effect was observed when control CETP was incubated with neuraminidase, an enzyme which is known to remove sialic acid from glycoproteins. CONCLUSIONS: We conclude that CETP from alcohol abusers may have a glycosylation defect due to defective sialylation caused posttranslationally by alcohol itself or its metabolite acetaldehyde. The defective glycosylation of CETP associated with altered binding to lipoproteins may lead to the low CETP activity observed previously in alcoholic subjects.
PubMed ID
16203750 View in PubMed
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Effects of ethanol on lipids and atherosclerosis.

https://arctichealth.org/en/permalink/ahliterature9519
Source
Pathophysiology. 2004 Apr;10(2):93-103
Publication Type
Article
Date
Apr-2004
Author
Minna L Hannuksela
Maria E Rämet
Antti E T Nissinen
Marja K Liisanantti
Markku J Savolainen
Author Affiliation
Department of Internal Medicine and Biocenter Oulu, University of Oulu, P.O. Box 5000, FIN-90014 Oulu, Finland.
Source
Pathophysiology. 2004 Apr;10(2):93-103
Date
Apr-2004
Language
English
Publication Type
Article
Abstract
Moderate alcohol consumption is associated with an increase in plasma high density lipoprotein (HDL) cholesterol concentration and a decrease in low density lipoprotein (LDL) cholesterol concentration. Changes in the concentration and composition of lipoproteins are estimated to account for more than half of alcohol's protective effect for coronary heart disease. Alcohol intake also affects plasma proteins involved in lipoprotein metabolism: cholesteryl ester transfer protein, phospholipid transfer protein, lecithin:cholesterol acyltransferase, lipoprotein lipase, hepatic lipase, and phospholipases. In addition, alcohol intake may result in acetaldehyde modification of apolipoproteins. Furthermore, "abnormal" lipids, phosphatidylethanol and fatty acid ethyl esters are formed in the presence of ethanol and are associated with lipoproteins in plasma. Ethanol and ethanol-induced modifications of lipids may modulate the effects of lipoproteins on the cells in the arterial wall. The molecular mechanisms involved in these processes are complex, requiring further study to better understand the specific effects of ethanol in the pathogenesis of atherosclerosis. This review discusses the effects of ethanol on lipoproteins and lipoprotein metabolism, as well as the novel effects of lipoproteins on vascular wall cells.
PubMed ID
15006415 View in PubMed
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Lipoprotein-associated phosphatidylethanol increases the plasma concentration of vascular endothelial growth factor.

https://arctichealth.org/en/permalink/ahliterature9489
Source
Arterioscler Thromb Vasc Biol. 2004 Jun;24(6):1037-42
Publication Type
Article
Date
Jun-2004
Author
Marja K Liisanantti
Minna L Hannuksela
Maria E Rämet
Markku J Savolainen
Author Affiliation
Department of Internal Medicine, University of Oulu, Oulu, Finland.
Source
Arterioscler Thromb Vasc Biol. 2004 Jun;24(6):1037-42
Date
Jun-2004
Language
English
Publication Type
Article
Keywords
Adult
Alcohol Drinking
Alcoholism - blood
Animals
Arteriosclerosis - prevention & control
Biological Transport - drug effects
Endothelium, Vascular - drug effects - secretion
Ethanol - pharmacology
Humans
Lipoproteins, HDL - chemistry
MAP Kinase Signaling System - drug effects
Male
Middle Aged
Models, Biological
Phosphatidylinositols - pharmacology
Rats
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Vascular Endothelial Growth Factor A - blood - secretion
Abstract
OBJECTIVE: To study whether qualitative changes in high-density lipoprotein (HDL) phospholipids mediate part of the beneficial effects of alcohol on atherosclerosis, we investigated whether phosphatidylethanol (PEth) in HDL particles affects the secretion of vascular endothelial growth factor (VEGF) from endothelial cells. METHODS AND RESULTS: PEth increased the secretion of VEGF into the culture medium of EA.hy 926 endothelial cells. The mitogen-activated protein kinase (MAPK) phosphorylation increased by 3.3-fold and protein kinase C (PKC) by 2.2-fold by PEth-containing HDL. Moreover, we showed that intravenous injection of PEth incorporated into HDL particles increased plasma concentration of VEGF by 2.4-fold in rats in vivo. Similar effect was observed when the rats were injected with HDL particles isolated from alcohol drinkers. CONCLUSIONS: HDL particles containing PEth affect endothelial cells by MAPK and PKC signaling. This may mediate the effects of ethanol on the arterial wall by increasing VEGF secretion from endothelial vascular cells. That may explain, at least in part, the beneficial effect of moderate alcohol consumption on atherosclerosis.
PubMed ID
15087306 View in PubMed
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