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Effect of n−3 fatty acids on the key enzymes involved in cholesterol and triglyceride turnover in rat liver
Author(s) -
AlShurbaji Ayman,
LarssonBackström Carin,
Berglund Lars,
Eggertsen Gösta,
Bjökhem Ingemar
Publication year - 1991
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02537204
Subject(s) - cholesterol , triglyceride , biochemistry , chemistry , coconut oil , sterol o acyltransferase , reductase , fatty acid , clinical chemistry , sunflower oil , medicine , endocrinology , enzyme , biology , lipoprotein
The effect of long‐chain n−3 fatty acids on hepatic key enzymes of cholesterol metabolism and triglyceride biosynthesis was investigated in two rat models. In the first model, rats were intravenously infused for two weeks with a fat emulsion containing 20% of triglycerides in which either n−6 or n−3 fatty acids predominated. The treatment with n−3 fatty acids led to a reduction primarily of serum cholesterol (45%), but also of serum triglycerides (18%). HMG‐CoA reductase activity and cholesterol 7α‐hydroxylase activity were reduced by 45% and 36%, respectively. There were no significant effects on diacylglycerol acyltransferase (DGAT) or phosphatidate phosphohydrolase (PAP) activities. In the second model, rats were fed a diet enriched with sucrose, coconut oil and either sunflower oil (n−6 fatty acids) or fish oil (long‐chain n−3 fatty acid ethyl esters). The treatment with n−3 fatty acids decreased serum triglycerides (41%) and, to a lesser extent, serum cholesterol (17%). Neither glycerol 3‐phosphate acyltransferase (GPAT) or DGAT were affected by n−3 fatty acids. In contrast, PAP activity was reduced by 26%. HMG‐CoA reductase was not significantly affected, whereas cholesterol 7α‐hydroxylase activity was reduced by 36%. The results indicate that part of the TG‐lowering effect of long‐chain n−3 fatty acids may be mediated by inhibition of the soluble phosphatidate phosphohydrolase. The effect on serum cholesterol may be partly due to inhibition of HMG‐CoA reductase.