Circulating ethanol does not stimulate pancreatic secretion in conscious rats

Area of Science:

• Gastroenterology
• Endocrinology
• Pharmacology

Background:

• Ethanol consumption is widespread, and its effects on pancreatic function are not fully understood.
• Previous research suggests potential roles for ethanol in pancreatic secretion, but findings are inconsistent.
• Investigating ethanol's direct impact on the pancreas is crucial for understanding alcohol-related gastrointestinal effects.

Purpose of the Study:

• To determine if circulating ethanol stimulates pancreatic secretion.
• To investigate whether ethanol augments stimulated pancreatic secretion.
• To elucidate the mechanism of ethanol-induced pancreatic secretion.

Main Methods:

• Awake, recovered rats underwent intravenous (IV) and intraduodenal (ID) ethanol infusions.
• Blood ethanol concentrations were maintained at approximately 0.1 mg% via IV infusion.
• Pancreatic protein and fluid secretion were measured, and the effect of ethanol on camostat-stimulated secretion was assessed.
• The role of cholecystokinin (CCK) was evaluated using a CCK receptor antagonist (CR1409).

Main Results:

• Intravenous ethanol infusion at 0.1 mg% did not significantly increase pancreatic secretion.
• Elevated circulating ethanol (0.1 mg%) did not affect camostat-stimulated pancreatic secretion.
• Intraduodenal ethanol infusion significantly stimulated pancreatic secretion at blood concentrations >= 0.19 mg%.
• This intraduodenal ethanol-induced secretion was completely blocked by the CCK receptor antagonist CR1409.

Conclusions:

• Circulating ethanol does not stimulate pancreatic secretion in rats.
• Intraduodenal ethanol administration potently stimulates pancreatic secretion.
• The pancreatic response to intraduodenal ethanol is mediated by cholecystokinin (CCK) release and receptor activation.