Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1975-11-6
pubmed:abstractText
To study possible factors in the pathogenesis of the ethanol-induced fatty liver, we investigated the effect of chronic ethanol consumption on the metabolism of fatty acids by isolated hepatic mitochondria. Chronic ethanol consumption resulted in decreased fatty acid oxidation, as evidenced by a reduction in oxygen uptake and CO2 production associated with the oxidation of fatty acids. The State 3 rate of oxygen uptake was depressed to a greater extent than the State 4 or the uncoupler-stimulated rate; the respiratory control ratio was also decreased. Therefore, one site of action of chronic ethanol feeding is on oxidative phosphorylation. The reduction in fatty acid oxidation, in general, is not due to an effect on the activation or translocation of fatty acids into the mitochondria. There was no effect by ethanol feeding on the activity of palmitoyl coenzyme A synthetase, whereas carnitine palmitoyltransferase activity was increased. The use of an artificial system (formazan production) to study beta oxidation in the absence of the electron transport chain is described. In the presence of fluorocitrate, which inhibits citric acid cycle activity, ketogenesis and formazan production were increased by chronic ethanol consumption. Thus beta oxidation to the level of acetyl-CoA is not impaired by chronic ethanol consumption. Total oxidation of fatty acids to CO2 is depressed by chronic ethanol intoxication because of effects on oxidative phosphorylation or the citric acid cycle (or both). Neither nutritional deficiency, cofactor depletion, nor the presence of ethanol in vitro explains these effects. Several of the effects of chronic ethanol consumption on fatty acid oxidation are mimicked by acetaldehyde and acetate, products of ethanol oxidation. Chronic ethanol consumption leads to persistent impairment of mitochondrial oxidation of fatty acids to CO2. However, oxidation of fatty acids to acetyl-CoA is not decreased by chronic ethanol consumption.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Caprylates, http://linkedlifedata.com/resource/pubmed/chemical/Carbon Dioxide, http://linkedlifedata.com/resource/pubmed/chemical/Carbon Radioisotopes, http://linkedlifedata.com/resource/pubmed/chemical/Carnitine O-Palmitoyltransferase, http://linkedlifedata.com/resource/pubmed/chemical/Citrates, http://linkedlifedata.com/resource/pubmed/chemical/Coenzyme A Ligases, http://linkedlifedata.com/resource/pubmed/chemical/Ethanol, http://linkedlifedata.com/resource/pubmed/chemical/Fatty Acids, http://linkedlifedata.com/resource/pubmed/chemical/Formazans, http://linkedlifedata.com/resource/pubmed/chemical/Ketone Bodies, http://linkedlifedata.com/resource/pubmed/chemical/Oleic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Palmitic Acids
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
250
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5122-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1975
pubmed:articleTitle
Effect of chronic ethanol ingestion on fatty acid oxidation by hepatic mitochondria.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.