Ethanol and lipid metabolism Differential effects on liver and brain microsomes

Sanchez-Amate, M.C.; Zurera, Jesús M.; Carrasco, Marı́a P.; Segovia, J.L.; Marco, Carmen

doi:10.1016/0014-5793(91)81190-j

Cited by 20 publications

(11 citation statements)

References 25 publications

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“…Regarding the synthesis of esterified cholesterol from oleate, the results set out in Table 4 show that the levels of radioactivity from oleate in the hepatocytes of rats fed with ethanol were 70% higher than in those of the controls. These results agree with those of other authors in rat liver [29] and chicken liver [30], where chronic alcohol administration was reported to increase the activity of acyl CoA:cholesterol acyltransferase (ACAT), the microsomal enzyme responsible for the esterification of cholesterol. This enzyme acylates endogenous free cholesterol and thus an increase in its activity may merely reflect greater substrate availability.…”

Section: Resultssupporting

confidence: 83%

Chronic ingestion of ethanol stimulates lipogenic response in rat hepatocytes

2001

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We isolated hepatocytes from rats chronically fed with ethanol and pair-fed control rats and incubated them both in the presence and absence of 100 mM ethanol in order to analyze the uptake into their lipids of several radiolabeled exogenous substrates. The hepatocytes treated chronically with ethanol showed higher lipogenic activity both in neutral lipids and phospholipids from serine, ethanolamine, glycerol and oleate. The only exception found was in the incorporation of choline into phosphatidylcholine (PC), which was lower in the hepatocytes from ethanol-fed rats than in the controls and was concomitant with a decrease in the PC levels of the ethanol-fed hepatocytes. The results obtained after exposing the cells to 100 mM ethanol in vitro indicate that in general the hepatocytes from ethanol-fed rats exhibit a higher lipogenic activity than the control cells. The only difference in the response to ethanol in vitro was found in the biosynthesis of phosphatidylserine (PS) from serine, which rose significantly in control cells but was unaffected in alcoholic hepatocytes. We put this difference in response down to specific adaptation to ethanol feeding.

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Section: Resultssupporting

confidence: 83%

Chronic ingestion of ethanol stimulates lipogenic response in rat hepatocytes

2001

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“…Membranes isolated from chronically ethanol-treated mice proved resistant to the fluidizing effect of ethanol (Chin and Goldstein 1977), and in parallel, the cholesterol content of the membranes was increased (Chin et al 1978). Chronic ethanol treatment also induced a significantly increased cholesterol level in microsomes isolated from chicken brain and liver (Sanchez-Amate et al 1991). Erythrocyte membranes isolated from chronic alcoholics exhibited an increase in cholesterol content and a decrease in membrane fluidity (Parmahamsa et al 2004).…”

Section: Heat Shock Proteins and Their Roles In Membrane Protectionmentioning

confidence: 99%

Alcohol stress, membranes, and chaperones

Tóth

Vı́gh

Sántha

2014

Cell Stress and Chaperones

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Ethanol, which affects all body organs, exerts a number of cytotoxic effects, most of them independent of cell type. Ethanol treatment leads to increased membrane fluidity and to changes in membrane protein composition. It can also interact directly with membrane proteins, causing conformational changes and thereby influencing their function. The cytotoxic action may include an increased level of oxidative stress. Heat shock protein molecular chaperones are ubiquitously expressed evolutionarily conserved proteins which serve as critical regulators of cellular homeostasis. Heat shock proteins can be induced by various forms of stresses such as elevated temperature, alcohol treatment, or ischemia, and they are also upregulated in certain pathological conditions. As heat shock and ethanol stress provoke similar responses, it is likely that heat shock protein activation also has a role in the protection of membranes and other cellular components during alcohol stress.

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“…The formation of the phospholipid phosphatidylethanol (PEth) during ethanol exposure has been implicated in the pathogenesis of alcohol-induced organ damage [7]. Hepatic triacylglycerol accumulations have been described in chronic alcoholism [12]; however, reports on the effects of ethanol administration on the biosynthesis of cellular phospholipids are few and contradictory [4,10,16]. Several researchers have found that ethanol affects the incorporation and distribution of various exogenously supplied substrates in different ways.…”

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confidence: 99%

Metabolic Fate of [<sup>14</sup>C]-Ethanol into Endothelial Cell Phospholipids Including Platelet-Activating Factor, Sphingomyelin and Phosphatidylethanol

Magai

Shukla²

2001

J Biomed Sci

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The metabolic fate of ethanol into the phospholipid pool of calf pulmonary artery endothelial cells was studied. [¹⁴C]-ethanol was incorporated into various endothelial cell phospholipids including phosphatidylethanol (PEth), which may represent a substantial fraction in microdomains of membrane phospholipids. The incorporation into phospholipids was reduced in the presence of pyrazole and cyanamide, inhibitors of ethanol metabolism. Wortmannin, the phosphatidylinositol 3-kinase inhibitor, increased [¹⁴C]-PEth formation. [³H]-acetate was also incorporated into endothelial cell phospholipids but in a different pattern. Distribution of [³H]-acetate and [¹⁴C]-ethanol into the fatty acyl moiety versus the glycerophosphoryl backbone of the phospholipids was also different. Stimulation of the endothelial cells with ATP increased [³H]-acetate incorporation into platelet-activating factor (PAF) and ethanol decreased it. Ethanol exposure increased ATP-stimulated [³H]-acetate incorporation into sphingomyelin. However, ATP had no effect on the incorporation of [¹⁴C]-ethanol into any phospholipids. The results suggest that the two precursors contribute to a separate acetate pool and that the sphingomyelin cycle may be sensitized in ethanol-treated cells. Thus, metabolic conversions of ethanol into lipids and the effect of ethanol on specific lipid mediators, e.g PAF, PEth and sphingomyelin, may be critical determinants in the altered responses of the endothelium in alcoholism.

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Ethanol and lipid metabolism Differential effects on liver and brain microsomes

Cited by 20 publications

References 25 publications

Chronic ingestion of ethanol stimulates lipogenic response in rat hepatocytes

Chronic ingestion of ethanol stimulates lipogenic response in rat hepatocytes

Alcohol stress, membranes, and chaperones

Metabolic Fate of [<sup>14</sup>C]-Ethanol into Endothelial Cell Phospholipids Including Platelet-Activating Factor, Sphingomyelin and Phosphatidylethanol

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