Impact of essential fatty acid deficiency on hepatic sterol metabolism in rats
β Scribed by E Levy; C Garofalo; T Rouleau; V Gavino; M Bendayan
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 815 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0270-9139
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β¦ Synopsis
EFA in the major mechanisms involved in the mainte-The major aim of the current investigation was to denance of hepatocyte sterol balance. (HEPATOLOGY fine whether essential fatty acid (EFA) deficiency modi-1996;23:848-857.) fies the intrahepatic metabolism and biliary output of sterols in rats. EFA-deficient diet caused an impoverishment in linoleic, arachidonic, and docosahexaenoic
The liver obviously plays a central role in cholesterol acids, and a marked enrichment in the eicosatrienoic homeostasis. 1 It constitutes the major site of lipogenacid of the plasma, liver, and hepatic microsomes. Duresis and very-low-density lipoprotein production, with ing a short term of biliary drainage, a significant decline the ability to form a portion of high-density lipoproof the pool size of biliary sterols was noted in EFA-defiteins. Conversely, the liver takes up and degrades varicient rats compared with control rats. To assess the bioous types of lipoproteins, including chylomicron remsynthesis of biliary components, the common bile duct nants and intermediate-, low-, and high-density was cannulated and the pool size depleted (24 hours). lipoproteins. In the hepatic parenchymal cells, cho-Subsequently, a 6-hour bile collection disclosed a signifilesterol is converted into bile acids, and the biliary secant decrease (nmoles/min/g liver) in bile acids (4.8 { 0.3 vs. 8.4 { 0.7, P Γ΅ .005), cholesterol (0.26 { 0.01 vs. 0.34 cretion of cholesterol, either in unchanged form or as { 0.02, P Γ΅ .05), and phospholipids (1.49 { 0.11 vs. 2.82 bile acids, represents the main physiological route of { 0.32, P Γ΅ .005) in EFA-deficient rats compared with net cholesterol elimination from the body. 4,5 controls (n Γ 6/group). When cholesterogenesis was mea-Abbreviations: HMG-CoA, hydroxymethylglutaryl-coenzyme A; ACAT, mental essential fatty acids (EFA) from which all othacyl-coenzyme A: cholesterol acyltransferase; EFA, essential fatty acids; cAMP, cyclic adenosine monophosphate; ATP, adenosine triphosphate. ers are derived by metabolic chain elongation and de-From the Departments of 1 Nutrition and 2 Anatomy, Centre de Recherche, saturation. The precursors are linoleic (v6) and
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High-density lipoprotein (HDL) participates in the transfer of cholesterol to the liver, in which it is subsequently excreted into bile as bile acid and cholesterol. In this study, the effect of essential fatty-acid (EFA) deficiency on cholesterol contribution from HDL subfractions to bile was inves
Hepatic mitochondrial functions related to fatty acid metabolism, including the respiratory control ratio, fatty acid oxidative capacity and carnitine palmitoyltransferase I activity, were studied in vitro with mitochondria isolated from rats treated with thioacetamide for up to 12 wk. The levels of
## Abstract Liver plasma membranes (LPM) were isolated from rats fed an essential fatty acidβsupplemented diet (+EFA) or from rats fed an essential fatty acidβdeficient diet (βEFA). The proportions of linoleate and arachidonate in membrane total fatty acids in the βEFA preparations were oneβhalf or