Investigating the Pathobiology of Alcoholic Pancreatitis
Version of Record online: 1 FEB 2011
Copyright © 2011 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 35, Issue 5, pages 830–837, May 2011
How to Cite
Pandol, S. J., Lugea, A., Mareninova, O. A., Smoot, D., Gorelick, F. S., Gukovskaya, A. S. and Gukovsky, I. (2011), Investigating the Pathobiology of Alcoholic Pancreatitis. Alcoholism: Clinical and Experimental Research, 35: 830–837. doi: 10.1111/j.1530-0277.2010.01408.x
- Issue online: 26 APR 2011
- Version of Record online: 1 FEB 2011
- Received for publication April 9, 2010; accepted June 18, 2010.
- Alcoholic Pancreatitis;
- Mitochondrial Permeabilization;
- Endoplasmic Reticulum Stress;
- Pancreatic Stellate Cell
Alcohol abuse is one of the most common causes of pancreatitis. The risk of developing alcohol-induced pancreatitis is related to the amount and duration of drinking. However, only a small portion of heavy drinkers develop disease, indicating that other factors (genetic, environmental, or dietary) contribute to disease initiation. Epidemiologic studies suggest roles for cigarette smoking and dietary factors in the development of alcoholic pancreatitis. The mechanisms underlying alcoholic pancreatitis are starting to be understood. Studies from animal models reveal that alcohol sensitizes the pancreas to key pathobiologic processes that are involved in pancreatitis. Current studies are focussed on the mechanisms responsible for the sensitizing effect of alcohol; recent findings reveal disordering of key cellular organelles including endoplasmic reticulum, mitochondria, and lysosomes. As our understanding of alcohol’s effects continue to advance to the level of molecular mechanisms, insights into potential therapeutic strategies will emerge providing opportunities for clinical benefit.