Document Detail


Effects of dietary polyunsaturated fatty acids and hepatic steatosis on the functioning of isolated working rat heart under normoxic conditions and during post-ischemic reperfusion.
MedLine Citation:
PMID:  11693187     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The purpose of this study was to modify the amount of 22:4 n-6, 22:5 n-6 and 20:5 n-3 in cardiac phospholipids and to evaluate the influence of these changes on the functioning of working rat hearts and mitochondrial energy metabolism under normoxic conditions and during postischemic reperfusion. The animals were fed one of these four diets: (i) 10% sunflower seed oil (SSO); (ii) 10% SSO + 1% cholesterol; (iii) 5% fish oil (FO, EPAX 3000TG, Pronova) + 5% SSO; (iv) 5% FO + 5% SSO + 1% cholesterol. Feeding n-3 PUFA decreased n-6 PUFA and increased n-3 PUFA in plasma lipids. In the phospholipids of cardiac mitochondria, this dietary modification also induced a decrease in the n-6/n-3 PUFA ratio. Cholesterol feeding induced marked hepatic steatosis (HS) characterized by the whitish appearance of the liver. It also brought about marked changes in the fatty acid composition of plasma and mitochondrial phospholipids. These changes, characterized by the impairment of deltaS- and delta6-desaturases, were more obvious in the SSO-fed rats, probably because of the presence of the precursor of the n-6 family (linoleate) in the diet whereas the FO diet contained large amounts of eicosapentaenoic and docosahexaenoic acids. In the mitochondrial phospholipids of SSO-fed rats, the (22:4 n-6 + 22:5 n-6) to 18:2 n-6 ratio was decreased by HS, without modification of the proportion of 20:4 n-6. In the mitochondrial phospholipids of FO-fed rats, the amount of 20:5 n-3 tended to be higher (+56%). Cardiac functioning was modulated by the diets. Myocardial coronary flow was enhanced by HS in the SSO-fed rats, whereas it was decreased in the FO-fed animals. The rate constant k012 representing the activity of the adenylate kinase varied in the opposite direction, suggesting that decreased ADP concentrations could cause oxygen wasting through the opening of the permeability transition pore. The recovery of the pump function tended to be increased by n-3 PUFA feeding (+22%) and HS (+45%). However, the release of ascorbyl free radical during reperfusion was not significantly modified by the diets. Conversely, energy production was increased by ischemia/reperfusion in the SSO group, whereas it was not modified in the FO group. This supports greater ischemia/reperfusion-induced calcium accumulation in the SSO groups than in the FO groups. HS did not modify the mitochondrial energy metabolism during ischemia/reperfusion. Taken together, these data suggest that HS- and n-3 PUFA-induced decrease in 22:4 and 22:5 n-6 and increase in 20:5 n-3 favor the recovery of mechanical activity during post-ischemic reperfusion.
Authors:
L Demaison; D Moreau; C Vergely-Vandriesse; S Grégoire; M Degois; L Rochette
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  224     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-11-05     Completed Date:  2002-03-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  103-16     Citation Subset:  IM    
Affiliation:
INRA, Unité de Nutrition Lipidique, Dijon, France.
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MeSH Terms
Descriptor/Qualifier:
Adenine / metabolism
Animals
Aorta / drug effects,  physiology
Ascorbic Acid / metabolism
Body Weight / drug effects
Cardiac Output / drug effects
Cell Respiration / drug effects
Cholesterol, Dietary / pharmacology
Coronary Circulation / drug effects
Dietary Fats / blood,  pharmacology*
Fatty Acids, Unsaturated / blood,  pharmacology*
Fish Oils / pharmacology
Free Radicals / metabolism
Heart / drug effects*,  physiology
Liver / drug effects,  metabolism,  pathology*
Mitochondria, Heart / chemistry,  drug effects*,  metabolism
Myocardial Ischemia / metabolism*,  pathology
Organ Size / drug effects
Oxygen / pharmacology
Palmitoylcarnitine / metabolism
Phosphates / metabolism
Plant Oils / pharmacology
Pyruvic Acid / metabolism
Rats
Reperfusion Injury / metabolism*,  pathology
Chemical
Reg. No./Substance:
0/Cholesterol, Dietary; 0/Dietary Fats; 0/Fatty Acids, Unsaturated; 0/Fish Oils; 0/Free Radicals; 0/Phosphates; 0/Plant Oils; 127-17-3/Pyruvic Acid; 1935-18-8/Palmitoylcarnitine; 50-81-7/Ascorbic Acid; 73-24-5/Adenine; 7782-44-7/Oxygen; 8001-21-6/sunflower seed oil

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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