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4. 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.)

Published
1991

9. 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

Published
1978
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10. 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.

Published
1991

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