Document Detail


Dietary phospholipid-dependent reductions in gene expression and activity of liver enzymes in fatty acid synthesis in fasted-refed rats.
MedLine Citation:
PMID:  10524348     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effects of dietary soybean phospholipid, its hydrogenation product and safflower phospholipid on gene expression and the activity of hepatic enzymes in fatty acid biosynthesis were examined in fasted-refed rats. Phospholipid composition of soybean phospholipid and its hydrogenation product were the same, but the hydrogenation product contained negligible amounts of unsaturated fatty acids. Among phospholipid classes, lysophosphatidylcholine and phosphatidylinositol proportions were slightly higher in safflower phospholipid than in soybean phospholipid or its hydrogenation product. Rats were fasted for 2 d and refed a fat-free diet or a diet containing 4% fatty acids either as soybean oil or various phospholipid preparations for 3 d. Compared to the fat-free diet, the soybean oil diet only slightly decreased specific, but not total hepatic fatty acid synthetase and malic enzyme activity, and it was totally ineffective in modulating glucose 6-phosphate dehydrogenase and pyruvate kinase activity under our experimental conditions. The diets containing phospholipids, however, markedly decreased the activity of these enzymes. The extent of reduction was somewhat attenuated with hydrogenated soybean phospholipid as compared with soybean and safflower phospholipids. Dot and Northern blot hybridization using specific cDNA probes showed that, compared to a fat-free diet, diets containing phospholipids profoundly decreased the hepatic mRNA levels of enzymes in fatty acid synthesis. Soybean oil, however, only marginally affected these parameters. Hepatic mRNA levels for enzymes correlated well with enzyme activity. Dietary phospholipids therefore appear to have decreased enzyme activity in fatty acid synthesis primarily by suppressing the mRNA levels of these enzymes. Compared to soybean oil, hydrogenated soybean phospholipid is still effective in decreasing the activity and mRNA level of enzymes in fatty acid synthesis. Therefore, it is difficult to ascribe the potent physiological activity of phospholipid in reducing fatty acid synthesis entirely to polyunsaturated fatty acid moiety.
Authors:
I A Rouyer; Y Takahashi; T Ide
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of nutritional science and vitaminology     Volume:  45     ISSN:  0301-4800     ISO Abbreviation:  J. Nutr. Sci. Vitaminol.     Publication Date:  1999 Jun 
Date Detail:
Created Date:  1999-11-17     Completed Date:  1999-11-17     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  0402640     Medline TA:  J Nutr Sci Vitaminol (Tokyo)     Country:  JAPAN    
Other Details:
Languages:  eng     Pagination:  287-302     Citation Subset:  IM    
Affiliation:
Laboratory of Nutrition Biochemistry, Ministry of Agriculture, Forestry and Fisheries, Tsukuba Science City, Ibaraki, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Dietary Fats, Unsaturated / pharmacology*
Fasting*
Fatty Acid Synthetase Complex / genetics,  metabolism
Fatty Acids / biosynthesis*
Food
Gene Expression / drug effects*
Glucosephosphate Dehydrogenase / genetics,  metabolism
Liver / enzymology*
Lysophosphatidylcholines / analysis,  pharmacology
Malate Dehydrogenase / genetics,  metabolism
Male
Phosphatidylinositols / analysis,  pharmacology
Phospholipids / pharmacology*
Pyruvate Kinase / genetics,  metabolism
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Safflower Oil / chemistry
Soybean Oil / chemistry
Chemical
Reg. No./Substance:
0/Dietary Fats, Unsaturated; 0/Fatty Acids; 0/Lysophosphatidylcholines; 0/Phosphatidylinositols; 0/Phospholipids; 0/RNA, Messenger; 8001-22-7/Soybean Oil; 8001-23-8/Safflower Oil; EC 1.1.1.37/Malate Dehydrogenase; EC 1.1.1.49/Glucosephosphate Dehydrogenase; EC 2.7.1.40/Pyruvate Kinase; EC 6.-/Fatty Acid Synthetase Complex

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


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