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3. Effect of ursodeoxycholic acid treatment on ileal absorption of bile acids in man as determined by the SeHCAT test

Author

Eusufzai, S., Ericsson, S., Cederlund, T., Einarsson, K., and Angelin, B.

Subjects
Bile acids -- Physiological aspects, Cholesterol -- Physiological aspects, Ursodiol -- Health aspects, Health
Abstract

Bile acids are produced by the liver and released into the small intestine in response to a meal; they aid in the efficient absorption of dietary fat and cholesterol. The bile acids are reabsorbed at a more distal point in the intestine, after they have accomplished their function, and return to the liver via the bloodstream where they await reentry into the cycle. The release and reabsorption of bile acids are part of a tightly controlled feedback cycle in which the rate of bile acid biosynthesis is regulated by both the demand for these compounds by the digestive tract and the rate at which they return to the liver. Ursodeoxycholic acid, a derivative of the major bile acids (and itself a minor constituent of bile) has been used in the treatment of a variety of disorders, including gall stones, primary biliary cirrhosis, and sclerosing cholangitis. The extent to which beneficial effects of ursodeoxycholic acid treatment may be related to its influence on intestinal absorption of bile acids is not known. To further investigate this issue, a newly available tracer technique involving monitoring the absorption of radioactively labelled selenium homocholic acid taurine (an easily measurable analog of naturally occurring bile acids) was used to quantify the effects of ursodeoxycholic acid on bile acid absorption. The radiolabelled acid was given orally, and bile acid absorption inferred from the rate of disappearance of radioactivity over a seven-day period. This was done before and after three weeks of treatment with ursodeoxycholic acid. Following treatment, there was a significant decrease in intestinal absorption of bile acids and blood cholesterol levels; blood levels of ursodeoxycholic acid increased. These results suggest that the beneficial effects of ursodeoxycholic acid treatment result, at least in part, from its suppressive actions on the absorption of bile acids. (Consumer Summary produced by Reliance Medical Information, Inc.) more...

Published
1991

8. Effects of Chenodeoxycholic Acid (CD) Treatment on Endogenous Plasma Triglyceride (TG) Transport in Hyperlipoproteinemia (HLP)

Author

Angelin, B., Einarsson, K., Leijd, B., Arreaza-Plaza, C. A., Otayek, M., Bosch, V., Avogaro, P., Bittolo-Bon, G., Pais, M., Taroni, G. C., Cazzolato, G., Quinci, G. B., Bateson, M. C., Bouchier, I. A. D., Bell, F. P., Quackenbush, F. W., Bentzen, C., Tourne, C., Wulfert, E., Bizzi, A., Garattini, S., Tacconi, A. M., Veneroni, E., Bjorkerud, S., Bondjers, G., Brattsand, R., Bylock, A., Hansson, G. K., Brindley, D. N., Burstein, M., Legmann, P., Aparicio, A. M., Boyle, E., Canosa, F. L., Cayen, M. N., Dvornik, D., Robinson, W. T., Cooper, E. E., Michel, A. M., Cowan, D. H., Robertson, A. L., Jr., Giroski, P., Shook, P., de Gennes, J. L., Piette, J. C., Piette, A. M., Truffert, J., DePalma, R. G., Bellon, E. M., Koletsky, S., Klein, L., Schneider, D. L., Ditschuneit, H. H., Klor, H. U., Ditschuneit, H., Drouin, P., Mejean, L., Wülfert, E., Eisele, B., Griss, G., Zimmer, A., Endo, A., Kitano, N., Fujii, S., Enomoto, H., Yoshikuni, Y., Ozaki, T., Zschocke, R., Ohata, K., Feldman, E. B., Gluck, F. B., Carter, A. C., Flanders, L., Nicholson, N., Fleischman, A. I., Bierenbaum, M. L., Stier, A., Fragiacomo, C., Lovati, M. R., Fox, U., Maione, G., Sirtori, C. R., Freeman, M. W., Spring-Mills, E., Jones, A. L., Gaion, R. M., Krishna, G., Galli, G., Galli-Kienle, M., Sanghvi, A., Gero, S., Szondy, E., Horvath, M., Fust, G., Szekely, J., Haacke, H., Parwaresch, M. R., Mader, Ch., Haller, H., Bruns, W., Michaelis, D., Schulze, J., Hanefeld, M., Leonhardt, W., Kemmer, C., Roschlau, G., Jaross, W., Hayes, T. M., Jones, A. W., Munn, J., Mottram, R., Hollander, W., Prusty, S., Nagraj, S., Kirkpatrick, B., Paddock, J., Colombo, M., Howard, A. N., Ghosh, P., Jackson, R. L., Kinnunen, P. K. J., Smith, L. E., Gotto, A. M., Jr., Sparrow, J. T., Jacotot, B., Girardet, M., Beaumont, J. L., Jaeger, H., Wechsler, J. G., Kabara, J. J., Vrable, R., Kanazawa, T., Terata, T., Komatsu, T., Izawa, M., Mori, H., Oike, Y., Metoki, H., Onodera, K., Ito, H., Izumiyama, S., Matsui, T., Kather, H., Simon, B., Kipshidze, N. N., Klimov, A. N., Sonina, S. I., Titova, G. V., Nagornev, V. A., Kobayakawa, T., Osuga, K., Yasuda, H., Kuzuya, F., Yoshimine, N., Lageron, A., Lang, P. D., Bablok, W., Endele, R., Koch, K., Stork, H., Schmidt, H. A. E., Lazarow, P. B., Lengsfeld, H., Brand, P., Baumgartner, H. R., Reber, K., Vecchi, M., Lithell, H., Boberg, J., Hellsing, K., Lundqvist, G., Vessby, B., Maebashi, M., Kawamura, N., Sato, M., Imamura, A., Malinow, M. R., McLaughlin, P., Stafford, C., Kohler, G. O., Livingston, A. L., Marmo, E., Vacca, C., Giordano, L., Schettino, A., Petrarca, R., Del Vecchio, F., Marshall, M., Hess, H., de Quiros, J. F. B., Mishkel, M. A., Crowther, S. M., Moltoni, D., Marinovich, M., Catapano, A., Ghiselli, G. C., Mordasini, R., Schlierf, G., Heuck, C. C., Oster, P., Schellenberg, B., Twelsick, H., Muller, K., Nakamura, H., Nagano, M., Olsson, A. G., Ballantyne, D., Carlson, L. A., Rossner, S., Walldius, G., Raetzer, H., Ostlund-Lindqvist, A.-M., Pollak, O. J., Prosdocimi, M., Caparrotta, L., Dorigo, P., Fassina, G., Puglisi, L., Maggi, F., Paoletti, R., Ferruti, P., Tanzi, M. C., Ramasarma, R., George, R., Oro, L., Rouffy, J., Chanu, B., Rousselet, F., Fredj, G., Clenet, M., Sarma, J. S. M., Bing, R. J., Sauvanet, J. P., Debry, G., Schade, R. W. B., Demacker, P., van’t Laar, A., Schaefer, E. J., Levy, R. I., Jenkins, L. L., Brewer, H. B., Jr., Schettler, G., Horsch, A. K., Schonborn, J., Heim, K., Schwartzkopff, W., Hoffmann, H., Njissen, J., Etzel, V., Zschiedrich, M., Simons, L. A., Isbister, J. P., Biggs, J. C., Stahelin, H. B., Keller, C., Mully, K., Reichlin, B., Berger, W., Story, J. A., Tepper, S. A., Kritchevsky, D., Subbiah, M. T. R., Sugano, M., Ikeda, I., Morioka, H., Thale, M., Faergeman, O., Tsushima, M., Hata, Y., Tsuchida, T., Irie, N., Goto, Y., Tulloch, B. R., Iype, P. T., Werner, I., Vogelberg, K. H., Cicmir, I., Koschinsky, Th., Greiser, E., Hutt, V., Kloer, H. U., Schoenborn, J., Weizel, A., Horsch, A., Wu, C.-C., Zimmerman, R., Hoffrichter, A., Walter, E., Ehlers, W., Andrassy, K., Weber, E., Kritchevsky, David, editor, Paoletti, Rodolfo, editor, and Holmes, William L., editor more...

Published
1978
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9. The Secretory Defect

Author

Einarsson, K., Angelin, B., Northfield, Tim, editor, Jazrawi, Riadh, editor, and Zentler-Munro, Patrick, editor

Published
1988
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17. [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. more...

Published
1991

20. 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. more...

Published
1997

49. Increased oxidoreduction of deoxycholic acid in cholecystectomised patients.

Author

Einarsson, K, Nilsell, K, and Björkhem, I

Abstract

The extent of oxidoreduction of deoxycholic acid in the enterohepatic circulation was studied in seven healthy subjects and seven patients after cholecystectomy. (12 beta-3H) Deoxycholic acid was given orally together with (24-14C) labelled bile acid. The rate of oxidoreduction of the 12 alpha-hydroxyl group of deoxycholic acid was calculated from the decay in ratio between 3H and 14C. In spite of a normal proportion of deoxycholic acid and other secondary bile acids in bile, patients after cholecystectomy had more than two-fold higher degree of oxidoreduction of the 12 alpha-hydroxyl group than healthy controls. The high extent of oxidoreduction is probably because of an increased exposure of the bile acid pool to intestinal bacteria and may have physiological implications. [ABSTRACT FROM PUBLISHER] more...

Published
1989

50. Mucin in gall bladder bile of gall stone patients: influence of treatment with chenodeoxycholic acid and ursodeoxycholic acid.

Author

Sahlin, S, Danielsson, A, Angelin, B, Reihnér, E, Henriksson, R, and Einarsson, K

Abstract

The concentration of hexosamine, a marker for mucin, was determined and related to the degree of cholesterol saturation and to the occurrence of cholesterol crystals in gall bladder bile of gall stone patients (n = 40) and gall stone free subjects (n = 25). Ten of the gall stone patients had been treated with chenodeoxycholic acid (CDCA) and eight with ursodeoxycholic acid (UDCA) three to four weeks before cholecystectomy. The hexosamine content was significantly higher in gall stone patients (137 (19) ng/ml, mean (SE) than in gall stone free subjects (83 (9) ng/ml, p less than 0.02). Treatment with CDCA or UDCA decreased cholesterol saturation, but did not significantly affect the hexosamine concentration. There was no difference in hexosamine concentration between gall stone patients with and without cholesterol crystals. The results do not support the hypothesis that the degree of cholesterol saturation is important for the mucin content of gall bladder bile in man. Neither do the data indicate that the formation and occurrence of cholesterol crystals in gall bladder bile from gall stone patients is caused by an increased concentration of mucin. As the studies were conducted on patients who had already had gall stones for several years, however, an effect of mucin in the very early stage of gall stone formation cannot be completely excluded. [ABSTRACT FROM PUBLISHER] more...

Published
1988
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