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Influence of bezafibrate on hepatic cholesterol metabolism in gallstone patients: Reduced activity of cholesterol 7α‐hydroxylase
Author(s) -
Ståhlberg Dagny,
Reihnér Eva,
Rudling Mats,
Berglund Lars,
Einarsson Kurt,
Angelin Bo
Publication year - 1995
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840210421
Subject(s) - bezafibrate , medicine , endocrinology , cholesterol , sterol o acyltransferase , reductase , clofibric acid , hydroxymethylglutaryl coa reductase , gemfibrozil , cholesterol 7 alpha hydroxylase , chemistry , hmg coa reductase , lipoprotein , enzyme , biochemistry
Bezafibrate is a hypolipidemic fibric acid derivative known to induce cholesterol supersaturation of bile. To characterize its effects on hepatic cholesterol metabolism, 31 normolipidemic, normal‐weight patients with gallstones undergoing cholecystectomy were studied. Eleven patients (5 men) were randomized to treatment with bezafibrate, 200 mg three times daily for 4 weeks before operation; the remaining 20 patients (5 men) served as nontreatment controls. At operation, a liver biopsy specimen was obtained under standardized conditions and several important parameters of cholesterol metabolism were assayed. Bezafibrate treatment lowered total plasma cholesterol and triglycerides 30% and 37%, respectively. The hepatic cholesterol 7α‐hydroxylasé activity was reduced by ≈60% in the bezafibrate treated patients compared with the controls, whereas the acyl‐coenzyme A: cholesterol acyltransferase (ACAT) activity was similar in the two groups. The total 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG CoA) reductase activity was increased twofold in the treated patients, whereas the active enzyme remained about the same as in the controls. The low‐density lipoprotein (LDL) receptor binding activity was unaffected by the treatment. Bezafibrate treatment significantly reduces cholesterol 7α‐hydroxylase activity, and it is suggested that this may play an important role for the development of supersaturated bile during such therapy. (H EPATOLOGY 1995; 21:1025–1030.)