BILE-SALTS STIMULATE GLYCOPROTEIN RELEASE BY GUINEA-PIG GALLBLADDER INVITRO

被引:16
作者
OLEARY, DP [1 ]
MURRAY, FE [1 ]
TURNER, BS [1 ]
LAMONT, JT [1 ]
机构
[1] UNIV HOSP BOSTON,EVANS MEM DEPT CLIN RES,GASTROENTEROL SECT,88 E NEWTON ST,BOSTON,MA 02118
关键词
D O I
10.1016/0270-9139(91)90270-6
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 [H-3]-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 gallbladder glycoprotein release in vitro by a detergent effect on the plasma membrane rather than by a receptor-mediated secretory pathway.
引用
收藏
页码:957 / 961
页数:5
相关论文
共 29 条
[1]   ANIONIC DETERGENTS AS DIVALENT-CATION IONOPHORES ACROSS BLACK LIPID-MEMBRANES [J].
ABRAMSON, JJ ;
SHAMOO, AE .
JOURNAL OF MEMBRANE BIOLOGY, 1979, 50 (3-4) :241-255
[2]  
AMADOR E, 1963, CLIN CHEM, V9, P391
[3]  
ARMSTRONG MJ, 1982, J LIPID RES, V23, P70
[4]  
BINDER HJ, 1975, GASTROENTEROLOGY, V68, P503
[5]  
BOUCHIER IA, 1965, GASTROENTEROLOGY, V49, P343
[6]   FORMATION OF ABNORMAL BILE AND CHOLESTEROL GALLSTONES FROM DIETARY CHOLESTEROL IN PRAIRIE DOG [J].
BRENNEMAN, DE ;
FORKER, EL ;
DENBESTEN, L ;
CONNOR, WE .
JOURNAL OF CLINICAL INVESTIGATION, 1972, 51 (06) :1495-+
[7]   PHARMACOLOGICAL INHIBITION OF CHENODEOXYCHOLATE-INDUCED FLUID AND MUCUS SECRETION AND MUCOSAL INJURY IN THE RABBIT COLON [J].
CAMILLERI, M ;
MURPHY, R ;
CHADWICK, VS .
DIGESTIVE DISEASES AND SCIENCES, 1982, 27 (10) :865-869
[8]  
Carey M. C., 1982, LIVER BIOL PATHOBIOL, P429
[9]   BILE-ACID STIMULATION OF COLONIC ADENYLATE-CYCLASE AND SECRETION IN RABBIT [J].
CONLEY, DR ;
COYNE, MJ ;
BONORRIS, GG ;
CHUNG, A ;
SCHOENFIELD, LJ .
AMERICAN JOURNAL OF DIGESTIVE DISEASES, 1976, 21 (06) :453-458
[10]  
FRESTON JW, 1969, GASTROENTEROLOGY, V57, P670