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Bile salts stimulate glycoprotein release by guinea pig gallbladder in vitro
Author(s) -
O'Leary Daniel P.,
Murray Francis E.,
Turner Bradley S.,
Lamont J. Thomas
Publication year - 1991
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.1840130526
Subject(s) - glycoprotein , biochemistry , chemistry , gallbladder , guinea pig , taurocholic acid , bile acid , biliary tract , medicine , biology , endocrinology
Alterations in the composition of bile during cholesterol gallstone formation appear to be responsible for increased release of gallbladder mucin, a potent cholesterol nucleating agent. We investigated the effects of bile salts on release of radiolabeled glycoproteins by explants of guinea pig gallbladder in organ culture. Bile salts, in concentrations of 1 to 5 mmol/L, caused a dose‐dependent release of [ 3 H]‐glycoproteins with a range of potencies in this order: chenodeoxycholate > deoxycholate > > cholate > ursodeoxycholate = control. Chenodeoxycholate and deoxycholate were significantly more potent than cholate (p < 0.0001). Unconjugated and taurine‐conjugated bile salts were of similar potency. Bile salts also caused increased release of glycoproteins from explants of guinea pig gastric antrum and colon. The bile salts released after bile salt exposure included mucin and lower molecular weight glycoproteins from the gallbladder. Release of glycoproteins in response to bile salts was not inhibited by indomethacin, atropine or propranolol, nor was it dependent on extracellular calcium or microtubules. Glycoprotein release in response to bile salts was associated with membrane damage as indicated by a dose‐dependent leakage of the cytoplasmic enzyme lactate dehydrogenase, although light microscopy did not reveal structural damage to epithelial cells. We conclude that hydrophobic bile salts stimulate gall‐bladder glycoprotein release in vitro by a detergent effect on the plasma membrane rather than by a receptor‐mediated secretory pathway. (H EPATOLOGY 1991;13:957–961.)