Journal of Lipid Research, Vol 22, 229-235, Copyright © 1981 by Lipid Research, Inc.
Dissociation of bile flow and biliary lipid secretion from biliary lysosomal enzyme output in experimental cholestasis
VH Lopez del Pino and NF LaRusso
Although the cellular mechanisms controlling bile flow and biliary lipid
secretion are unclear, morphologic data suggest that intracellular vesicles
may be involved. Therefore, to investigate the role of hepatocyte lysosomes
in bile flow and biliary lipid secretion, we studied the effect of
cholestasis on biliary lipid output and on lysosomal enzyme activities and
total protein concentration in liver and bile. Castrated male rats were
treated with ethinyl estradiol at 0.5 or 5 mg/kg per day for 5 days; bile
was collected through a complete bile fistula hourly for 4 hours, and then
liver homogenates were prepared. Bile acids, cholesterol, and phospholipid
were measured in bile, and three lysosomal glycosidases
(beta-glucuronidase, beta- galactosidase, and
N-acetyl-beta-glucosaminidase) and total protein were measured in bile and
liver. Ethinyl estradiol inhibited bile flow in a dose-dependent fashion;
it also inhibited bile acid and phospholipid outputs. In contrast, a marked
and parallel increase in the biliary outputs of all three lysosomal
hydrolases was observed after high-dose ethinyl estradiol; no change in the
biliary concentration of total protein was found. Our data suggest that
bile flow and biliary lipid secretion involve cellular mechanisms other
than vesicular transport by lysosomes.
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