Bilirubin overload modulates bile canalicular membrane fluidity in rats: association with disproportionate reduction of biliary lipid secretion

2000 ◽  
Vol 35 (6) ◽  
pp. 450-455 ◽  
Author(s):  
Tsuyoshi Kajihara ◽  
Susumu Tazuma ◽  
Gunji Yamashita ◽  
Goro Kajiyama
2001 ◽  
Vol 354 (3) ◽  
pp. 591-596 ◽  
Author(s):  
Shigeyuki YASUMIBA ◽  
Susumu TAZUMA ◽  
Hidenori OCHI ◽  
Kazuaki CHAYAMA ◽  
Goro KAJIYAMA

Changes of the biliary canalicular membrane lipid content can affect membrane fluidity and biliary lipid secretion in rats. The immunosuppressant cyclosporin A is known to cause intrahepatic cholestasis. This study investigated whether cyclosporin A influenced canalicular membrane fluidity by altering membrane phospholipids or transporter expression. In male Sprague–Dawley rats, a bile-duct cannula was inserted to collect bile, and sodium taurocholate was infused (100nmol/min per 100g) for 60min. During steady-state taurocholate infusion, cyclosporin A (20mg/kg) or vehicle was injected intravenously and then bile was collected for 80min. After killing the rats, canalicular membrane vesicles were prepared. Expression of canalicular membrane transporters was assessed by Western blotting and canalicular membrane vesicle fluidity was estimated by fluorescence polarization. Cyclosporin A reduced biliary lipid secretion along with a disproportionate reduction of lipids relative to bile acids. Cyclosporin A significantly decreased canalicular membrane fluidity along with an increase of the cholesterol/phospholipid molar ratio. Only expression of the transporter P-glycoprotein was increased by cyclosporin A. Because canalicular membrane transporter expression was largely unchanged by cyclosporin A despite a marked decrease of biliary lipid secretion, transporter activity may partly depend upon canalicular membrane fluidity.


1986 ◽  
Vol 234 (2) ◽  
pp. 421-427 ◽  
Author(s):  
K Rahman ◽  
T G Hammond ◽  
P J Lowe ◽  
S G Barnwell ◽  
B Clark ◽  
...  

A major determinant of biliary lipid secretion is bile-salt secretion. Taurocholate (TC), a micelle-forming bile salt, was infused continuously at different rates in both isolated perfused livers and biliary-fistula rats. In both of these systems, infusion of TC brought about an elevated secretion of phosphatidylcholine for the duration of the TC infusion period. Initial phospholipid/bile-salt ratios in the bile were higher in the whole-animal model than in isolated livers, but at the higher infusion rates both secreted approx. 6 mol of phospholipid for every 100 mol of bile salt. The secretion of phospholipid, which was maintained even at high rates of bile-salt infusion, suggest a continuous and regulated phospholipid supply and secretion mechanism. In contrast, however, multiple short pulses of TC to the perfused liver, which brought about relatively equal biliary bile-salt output pulses, did not bring about equal phospholipid outputs, since the phospholipid peak size declined with each bile-salt pulse. These experiments taken together suggest either that a threshold (intracellular) bile-salt concentration may be required to ‘switch-on’ the phospholipid supply and that it may need to be maintained for continuous biliary phospholipid supply to the canalicular membrane.


1996 ◽  
Vol 36 (10) ◽  
pp. 2147-2163 ◽  
Author(s):  
J M Crawford ◽  
G M Möckel ◽  
A R Crawford ◽  
S J Hagen ◽  
V C Hatch ◽  
...  

1992 ◽  
Vol 267 (25) ◽  
pp. 18093-18099
Author(s):  
E Buschman ◽  
R.J. Arceci ◽  
J.M. Croop ◽  
M Che ◽  
I.M. Arias ◽  
...  

2000 ◽  
Vol 118 (4) ◽  
pp. A1422
Author(s):  
Yasumasa Asamoto ◽  
Susumu Tazuma ◽  
Hidenori Ochi ◽  
Tsuyoshi Kajihara ◽  
Hideyuki Hyougo ◽  
...  

Author(s):  
Elena Bravo ◽  
Alfredo Cantafora ◽  
Carla Cicchini ◽  
Michael Avella ◽  
Kathleen M. Botham

1979 ◽  
Vol 56 (3) ◽  
pp. 22P-22P ◽  
Author(s):  
A. Reuben ◽  
P. N. Maton ◽  
Y. Quereshi ◽  
R. H. Dowling

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