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846 results on '"Angelin, B."'

105. [Effect of pravastatin on hepatic cholesterol metabolism]

Author

Reihnér E, Rudling M, Ståhlberg D, Berglund L, Ewerth S, Ingemar Björkhem, Einarsson K, and Angelin B

Subjects
Adult, Male, Middle Aged, Naphthalenes, Cholesterol, Liver, Receptors, LDL, Cholelithiasis, Heptanoic Acids, Humans, Female, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Aged, Pravastatin
Abstract

Inhibitors of the rate-limiting enzyme of cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are now used frequently to treat hypercholesterolemia. We studied the effects of specific inhibition of cholesterol synthesis by one of these agents (pravastatin) on the hepatic metabolism of cholesterol in patients with gallstone disease who were scheduled to undergo cholecystectomy.Ten patients were treated with pravastatin (20 mg twice a day) for three weeks before cholecystectomy; 20 patients not treated served as controls. A liver specimen was obtained from each patient at operation, and the activities of rate-determining enzymes in cholesterol metabolism as well as low-density-lipoprotein (LDL)-receptor binding activity were determined.Pravastatin therapy reduced plasma total cholesterol by 26 percent and LDL cholesterol by 39 percent (p less than 0.005). Serum levels of free lathosterol, a precursor of cholesterol whose concentration reflects the rate of cholesterol synthesis in vivo, decreased by 63 percent (p less than 0.005), indicating reduced de novo biosynthesis of cholesterol. Microsomal HMG-CoA reductase activity, when analyzed in vitro in the absence of the inhibitor, was increased 11.8-fold (1344 +/- 311 vs. 105 +/- 14 pmol per minute per milligram of protein in the controls; p less than 0.001). The expression of LDL receptors was increased by 180 percent (p less than 0.005), whereas the activities of cholesterol 7 alpha-hydroxylase (which governs bile acid synthesis) and of acyl-coenzyme A: cholesterol O-acyltransferase (which regulates cholesterol esterification) were unaffected by treatment.Inhibition of hepatic HMG-CoA reductase by pravastatin results in an increased expression of hepatic LDL receptors, which explains the lowered plasma levels of LDL cholesterol.

Published
1991

112. Secretion and composition of bile after human liver transplantation : studies on the effects of cyclosporine and tacrolimus

Author

Ericzon, B G, Eusufzai, S, Söderdahl, G, Duraj, Frans, Einarsson, K, Angelin, B, Ericzon, B G, Eusufzai, S, Söderdahl, G, Duraj, Frans, Einarsson, K, and Angelin, B

Abstract

Cyclosporine (CsA) and tacrolimus (FK506) have recently been reported to inhibit canalicular transport of bile acids in vitro and thereby possibly induce cholestasis. A relative reduction of chenodeoxycholic acid (CDCA) has been observed after liver transplantation when CsA is used as immunosuppressant. We tested the hypothesis that CsA induces cholestasis and reduces CDCA secretion as compared with treatment with monoclonal antibodies (OKT3), and that CsA differs from FK506 with regard to its effects on biliary lipid secretion. Bile flow, biliary lipid secretion rates, and biliary bile acid composition were determined during the first 10 days after transplantation in 29 liver transplant recipients. Two prospective randomized studies were performed that compared CsA and OKT3 and compared CsA- and FK506-based regimens. In study 1, bile acid output averaged 0.75±0.15 µmol/min in the CsA I group and 0.54±0.11 µmol/min in the OKT3 group on postoperative day 1. Bile flow and bile acid output then increased, and there was no significant difference between the two groups. The relative proportion of CDCA decreased to the same extent in both groups. In study 2, mean bile acid outputs on postoperative day 1 were 0.57±0.26 µmol/min and 0.55±0.15 µmol/min in the CsA 2 and FK506 groups, respectively. The following increase in bile acid secretion was significantly larger in the FK506 group. After transplantation, the relative proportion of CDCA decreased with time in both groups, but the reduction was more rapid in the FK506 group. In conclusion, CsA did not inhibit bile secretion during short-term treatment after liver transplantation. Compared with patients given CsA-based treatment, patients with FK506-based treatment recovered bile secretion more rapidly.

Published
1997

117. Expression of very low density lipoprotein receptor in the vascular wall. Analysis of human tissues by in situ hybridization and immunohistochemistry.

Author

Multhaupt, H A, Gåfvels, M E, Kariko, K, Jin, H, Arenas-Elliot, C, Goldman, B I, Strauss, J F, Angelin, B, Warhol, M J, McCrae, K R, Multhaupt, H A, Gåfvels, M E, Kariko, K, Jin, H, Arenas-Elliot, C, Goldman, B I, Strauss, J F, Angelin, B, Warhol, M J, and McCrae, K R

Abstract

Udgivelsesdato: 1996-Jun, The recently cloned very low density lipoprotein (VLDL) receptor binds triglyceride-rich, apolipoprotein-E-containing lipoproteins with high affinity. The observation that VLDL receptor mRNA is abundantly expressed in extracts of tissues such as skeletal muscle and heart, but not liver, has led to the hypothesis that this receptor may facilitate the peripheral uptake of triglyceride-rich lipoproteins. However, little information is available concerning the types of cells that express this receptor in vivo. As expression of the VLDL receptor in the vascular wall might have important implications for the uptake and transport of triglyceride-rich lipoproteins, and perhaps facilitate the development of atherosclerosis in hypertriglyceridemic individuals, we used in situ hybridization and immunohistochemistry to determine whether VLDL receptor mRNA and protein was expressed in human vascular tissue. We observed expression of the receptor by both endothelial and smooth muscle cells within normal arteries and veins, as well as within atherosclerotic plaques. In the latter, the VLDL receptor was also expressed by macrophage-derived foam cells. The widespread distribution of the VLDL receptor in vascular tissue suggests a potentially important role for this receptor in normal and pathophysiological vascular processes.

Published
1996

139. Cloning of a complementary deoxyribonucleic acid encoding the murine homolog of the very low density lipoprotein/apolipoprotein-E receptor: expression pattern and assignment of the gene to mouse chromosome 19".

Author

Gafvels, M E, primary, Paavola, L G, additional, Boyd, C O, additional, Nolan, P M, additional, Wittmaack, F, additional, Chawla, A, additional, Lazar, M A, additional, Bucan, M, additional, Angelin, B, additional, and Strauss, J F, additional

Published
1995
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142. Cloning of a complementary deoxyribonucleic acid encoding the murine homolog of the very low density lipoprotein/apolipoprotein-E receptor: expression pattern and assignment of the gene to mouse chromosome 19.

Author

Gåfvels, M E, primary, Paavola, L G, additional, Boyd, C O, additional, Nolan, P M, additional, Wittmaack, F, additional, Chawla, A, additional, Lazar, M A, additional, Bucan, M, additional, Angelin, B O, additional, and Strauss, J F, additional

Published
1994
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