Effects of ethanol on lipid metabolism.
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TLDR
The capacity of lipoprotein production and hyperlipemia development increases during chronic alcohol consumption, probably as a result of the concomitant hypertrophy of the endoplasmic reticulum and Golgi apparatus, however, this compensation is relatively inefficient in ridding the liver of fat.About:
This article is published in Journal of Lipid Research.The article was published on 1979-03-01 and is currently open access. It has received 351 citations till now. The article focuses on the topics: Fatty liver & Ethanol metabolism.read more
Citations
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Wine, alcohol, platelets, and the French paradox for coronary heart disease
Serge Renaud,M de Lorgeril +1 more
TL;DR: Data from Caerphilly, Wales, show that platelet aggregation, which is related to CHD, is inhibited significantly by alcohol at levels of intake associated with reduced risk of CHD.
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Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets
Bin Gao,Ramon Bataller +1 more
TL;DR: Findings from recent studies that have characterized specific intracellular signaling pathways, transcriptional factors, aspects of innate immunity, chemokines, epigenetic features, microRNAs, and stem cells that are associated with ALD are reviewed, improving the understanding of its pathogenesis.
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The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice
TL;DR: Adiponectin was effective in ameliorating hepatomegaly, steatosis, and alanine aminotransferase abnormality associated with nonalcoholic obese, ob/ob mice and could suppress the hepatic production of TNF-alpha and plasma concentrations of this proinflammatory cytokine.
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Dietary influences on serum lipids and lipoproteins.
Scott M. Grundy,Margo A. Denke +1 more
TL;DR: At present it appears that carbohydrates and monounsaturated fatty acids represent the preferred replacements for saturated fatty acids, although modest increases in polyunsaturated fatty acid and stearic acid, at the expense of cholesterol-raising saturates, probably are safe and may provide for greater variety in the diet.
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Effect of apoproteins on hepatic uptake of triglyceride emulsions in the rat.
TL;DR: In this article, Apoprotein E isolated from human very low density lipoproteins to both rat lymph chylomicrons and a triglyceride emulsion significantly increased the hepatic uptake of these particles in a nonrecycling isolated rat liver perftision system.
References
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Plasma-high-density-lipoprotein concentration and development of ischæmic heart-disease
G.J Miller,N.E Miller +1 more
TL;DR: The body cholesterol pool increases with decreasing plasma-high-density-lipoprotein (H.D.L.) but is unrelated to the plasma concentrations of total cholesterol and other lipoproteins, and it is proposed that a reduction of plasma-H.H.L.D., is reduced in several conditions associated with an increased risk of future ischaemic heart-disease, by impairing the clearance of cholesterol from the arterial wall.
Journal ArticleDOI
Atherosclerosis and the arterial smooth muscle cell: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis.
Russell Ross,John A. Glomset +1 more
Journal Article
Carbon tetrachloride hepatotoxicity
TL;DR: The knowledge that hepatic triglyceride secretion involves a dual mechanism has provided a powerful new guide for the analysis of mechanisms underlying fatty liver disease, and a central requirement of this hypothesis must be that if over supply of fatty acids is to be invoked as a significant factor in the pathogenesis of fatty liver, then the oversupply must be of sufficient magnitude and duration.
Journal Article
Classification of hyperlipidaemias and hyperlipoproteinaemias.
TL;DR: The present memorandum presents a classification of the main types of hyperlipidaemia, based on lipoprotein analyses by electrophoresis and ultracentrifugation, and briefly describes the criteria for diagnosis as well as the methods of their determination.
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Hepatic Microsomal Ethanol-oxidizing System: IN VITRO CHARACTERISTICS AND ADAPTIVE PROPERTIES IN VIVO
TL;DR: The existence of a microsomal ethanol-oxidizing system, especially its capacity to increase in activity adaptively after ethanol feeding, may explain various effects of ethanol, including proliferation of hepatic smooth endoplasmic reticulum, induction of other hepaticmicrosomal drug-detoxifying enzymes, and the metabolic tolerance to ethanol which develops in alcoholics.