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Articles in PresS, published online ahead of print December 19, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00388.2001
Submitted on August 31, 2001
Accepted on November 29, 2001
1 Medicine, VA Connecticut Healthcare, West Haven, CT, USA
2 Medicine, VA Connecticut Healthcare, West Haven, CT, USA; Medicine and Cell Biology, Yale Univesity, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: fred.gorelick{at}yale.edu.
Activation of zymogens within the pancreatic acinar cell is an early feature of acute pancreatitis. Supraphysiologic concentrations of cholecystokinin (CCK) cause zymogen activation and pancreatitis. The effects of the CCK analogue, cerulein, and alcohol on trypsin and chymotrypsin activation in isolated pancreatic acini were examined. Cerulein increased markers of zymogen activation in a time and concentration-dependent manner. Notably, trypsin activity reached a peak value within 30 min, then diminished with time while chymotrypsin activity increased with time. Ethanol [35 mM], a known cause of pancreatitis, sensitized the acinar cells to the effects of cerulein [10-9 to 10-7M] on zymogen activation, but had no effect alone. The effects of ethanol were concentration-dependent. Alcohols with a chain length of 
2 also sensitized the acinar cell to cerulein; the most potent was butanol. Branched alcohols, 2-propanol and 2-butanol, were less potent than their aliphatic counterparts, 1-propanol, 1-butanol. The structure of an alcohol is related to its ability to sensitize acinar cells to the effects of cerulein on zymogen activation.
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