A STUDY ON LIPID-METABOLISM IN HEART AND LIVER OF CHOLESTEROL-FED ANDPECTIN-FED RATS

Citation
S. Hexeberg et al., A STUDY ON LIPID-METABOLISM IN HEART AND LIVER OF CHOLESTEROL-FED ANDPECTIN-FED RATS, British Journal of Nutrition, 71(2), 1994, pp. 181-192
Citations number
32
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00071145
Volume
71
Issue
2
Year of publication
1994
Pages
181 - 192
Database
ISI
SICI code
0007-1145(1994)71:2<181:ASOLIH>2.0.ZU;2-7
Abstract
Pectin is known as a cholesterol-reducing dietary fibre, and in the pr esent study we addressed the question whether pectin affected the quan tity of lipid in droplets in the myocardial cells and of Lipid in the liver cells. Male Wistar rats received either a diet containing choles terol or a standard diet without cholesterol with 0, 50 or 100 g pecti n/kg incorporated for 10 d. The fractional volume of lipid droplets in the myocardial cells decreased as a function of pectin dose in both t he standard-fed and the cholesterol-fed rats. Serum cholesterol was si gnificantly reduced in both groups after addition of 100 g pectin/kg d iet. The cholesterol diet increased the liver cholesterol level, and 1 00 g pectin/kg diet resulted in a lower concentration of liver cholest erol in the cholesterol-fed animals, but the influence on standard-fed rats was modest. Hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88; HM G-CoA reductase) activity increased when pectin was given in the stand ard diet. Liver triacylglycerol level increased after cholesterol and pectin feeding. Mitochondrial fatty acid oxidation and phosphatidate p hosphohydrolase (EC3.1.3.4) activity tended to decrease, whereas the p eroxisomal fatty acid oxidation and acyl-CoA oxidase activity were unc hanged. Increased hepatic triacylglycerol content by cholesterol and p ectin treatment may be due to inhibited mitochondrial fatty acid oxida tion along with increased availability of fatty acid for esterificatio n and triacylglycerol synthesis. The presence of pectin in the diets o f cholesterol-fed rats resulted in increased hepatic concentration of triacylglycerols and increased mitochondrial fatty acid oxidation. In this case the hepatic accumulation of triacylglycerol may be mediated by a reduced efflux of triacylglycerols from the liver.