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Am J Physiol Gastrointest Liver Physiol 274: G1151-G1159, 1998;
0193-1857/98 $5.00
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Vol. 274, Issue 6, G1151-G1159, June 1998

Changes in G protein expression account for impaired modulation of hepatic cAMP formation after BDL

Bernard Bouscarel1,2, Yasushi Matsuzaki3, Man Le3, Thomas W. Gettys4, and Hans Fromm1

1 Division of Gastroenterology and Nutrition, Department of Medicine, and 2 Department of Biochemistry and Molecular Biology, The George Washington University Medical Center, Washington, District of Columbia 20037; 3 Division of Gastroenterology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki 305, Japan; and 4 Division of Gastroenterology, Departments of Medicine and of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425-2223

The regulation of cAMP synthesis by hormones and bile acids is altered in isolated hamster hepatocytes 2 days after bile duct ligation (BDL) [Y. Matsuzaki, B. Bouscarel, M. Le, S. Ceryak, T. W. Gettys, J. Shoda, and H. Fromm. Am. J. Physiol. 273 (Gastrointest. Liver Physiol. 36): G164-G174, 1997]. Therefore, studies were undertaken to elucidate the mechanism(s) responsible for this impaired modulation of cAMP formation. Hepatocytes were isolated 48 h after either a sham operation or BDL. Both preparations were equally devoid of cholangiocyte contamination. Although the basal cAMP level was not affected after BDL, the ability of glucagon to maximally stimulate cAMP synthesis was decreased by ~40%. This decreased glucagon effect after BDL was not due to alteration of the total glucagon receptor expression. However, this effect was associated with a parallel 50% decreased expression of the small stimulatory G protein alpha -subunit (Gsalpha S). The expression of either the large subunit (Gsalpha L) or the common beta -subunit remained unchanged. The expression of Gialpha 2 and Gialpha 3 was also decreased by 25 and 46%, respectively, and was associated with the failure of ANG II to inhibit stimulated cAMP formation. Therefore, alterations of the expression of Gsalpha S and Gialpha are, at least in part, responsible for the attenuated hormonal regulation of cAMP synthesis. Because cAMP has been reported to stimulate both bile acid uptake and secretion, impairment of cAMP synthesis and bile acid uptake may represent an initial hepatocellular defense mechanism during cholestasis.

bile acid; ursodeoxycholic acid; adenosine 3',5'-cyclic monophosphate; isolated hamster hepatocytes; cholestasis


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