Document Detail

Reduced postprandial serum paraoxonase activity after a meal rich in used cooking fat.
MedLine Citation:
PMID:  10323788     Owner:  NLM     Status:  MEDLINE    
Paraoxonase is an enzyme associated with HDL in human serum that hydrolyzes oxidized phospholipids and inhibits LDL oxidation, which is an important step in atherogenesis. In animals, addition of oxidized lipids to the circulation reduces paraoxonase activity, and diets rich in oxidized fat accelerate the development of atherosclerosis. The current randomized, crossover study was designed to compare the effect of a meal rich in oxidized lipids in the form of fat that had been used for deep-frying in a fast food restaurant and a control meal rich in the corresponding unused fat on postprandial serum paraoxonase (arylesterase) activity and peroxide content of LDL and its susceptibility to copper ion catalyzed oxidation in 12 healthy men. Four hours into the postprandial period, serum paraoxonase activity had decreased significantly after the used fat meal (-17%, P=0.005) and had increased significantly after the meal rich in unused fat (14%, P=0. 005). These changes were significantly (P=0.003) different. A time-course study indicated that serum paraoxonase activity remained lower than baseline for up to 8 hours after the used fat meal. Serum apoA1 concentration tended to decrease after the unused fat meal and tended to increase after the used fat meal. These changes were different at a marginal level of significance (P=0.07). Also, a significantly (P=0.03) greater decrease in apoA1 content of postprandial HDL was recorded after the unused fat meal. The peroxide content of LDL tended to decrease after the used fat meal and tended to increase after the control meal. These changes were significantly (P=0.04) different. Susceptibility of isolated LDL to copper ion oxidation and plasma levels of malondialdehyde were unchanged during the study. These data suggest that in the postprandial period after a meal rich in used cooking fat, the enzymatic protection of LDL against accumulation of peroxides and atherogenic oxidative modification may be reduced, possibly due to factors associated with apoA1, without acutely affecting the intrinsic resistance of LDL to in vitro oxidation.
W H Sutherland; R J Walker; S A de Jong; A M van Rij; V Phillips; H L Walker
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  19     ISSN:  1079-5642     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  1999 May 
Date Detail:
Created Date:  1999-06-07     Completed Date:  1999-06-07     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1340-7     Citation Subset:  IM    
Department of Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
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MeSH Terms
Antioxidants / metabolism
Apolipoprotein A-I / blood
Cookery / methods*
Cross-Over Studies
Dietary Fats / pharmacology*
Esterases / blood*
Fatty Acids / blood
Hot Temperature
Lipid Peroxidation*
Lipoproteins, HDL / blood*,  chemistry
Lipoproteins, LDL / blood*
Middle Aged
Phospholipids / blood
Vitamin E / blood
Reg. No./Substance:
0/Antioxidants; 0/Apolipoprotein A-I; 0/Dietary Fats; 0/Fatty Acids; 0/Lipoproteins, HDL; 0/Lipoproteins, LDL; 0/Phospholipids; 0/oxidized low density lipoprotein; 1406-18-4/Vitamin E; EC 3.1.-/Esterases; EC

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