Background/Aims:
@EN supplement of exogenous pancreatic enzyme is the only available method for the treatment of pancreatic insufficiency. Theoretically, it is rather a basic way to ameliorate symptoms of pancreatic insufficiency, if hypertrophy and/or
hyperplasia
could
be induced in exocrine pancreas. Therefore, exogenous or endogenous cholecystokinin (CCK) which induces hypertrophy and hyperplasia of the exocrine pancreas may increase pancreatic enzyme output in patients with pancreatic insufficiency. This
study
aimed to determine the effects of CCK or camostat, a protease inhibitor with endogenous CCK releasing effect, on pancreatic insufficiency in rat pancreatic insufficiency model.
@ES Methods:
@EN Male Sprague-Dawley rats were devided into 4 groups; control, insufficiency, inscufficiency ttcck and insufficiency tcamostat. Pancreatic insufficiency was produced by instillating oleic acid (25 ㎍/100g body weight) into the
pancreaticobiliary
duct
of rats. CCK (CCK-8, 10 ㎍/kg/day, s. c.) or camostat (200 mg/kg/day, i. g.) was given after oleic acid instillation.
@ES Results:
@EN Severe pancreatic insufficiency was developed within 3 days and maintained up to 2 weeks observed. The acini of the pancreas were progressively destroyed and showed fibrotic changes after oleic acid instillation, however, islet cells were
intact.
The amylase as well as trypsin output was decreased more than 90% of control at 1 week after induction of pancreatic insufficiency. The pancreatic enzyme secretion was minimally maintained in the insufficiency rats treated with CCK or camostat.
Further,
the acinar destruction was attenuated by CCK or camostat.
@ES Conclusions:
@EN These results strongly suggest that CCK or camostat improves the function of exocrine pancreas in pancreatic insufficiency. (Korean J Gastroenterol 1995;27: 96-109)
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