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World J Gastrointest Pharmacol Ther. Feb 6, 2010; 1(1): 3-8
Published online Feb 6, 2010. doi: 10.4292/wjgpt.v1.i1.3
Ethanol consumption as inductor of pancreatitis
José A Tapia, Ginés M Salido, Antonio González
José A Tapia, Ginés M Salido, Antonio González, PhD, Department of Physiology, Faculty of Veterinary Sciences, University of Extremadura, Avenida Universidad s/n, Cáceres E-10071, Spain
Author contributions: Tapia JA wrote part of the introduction and the text referring to inflammation and secretion; Salido GM contributed to the abstract, the introduction and corrections of the text; González A wrote the introduction, concluding remarks and the text referring to calcium homeostasis, oxidative stress and cell proliferation.
Supported by Junta de Extremadura-FEDER, PRI08A018
Correspondence to: Antonio González, PhD, Department of Physiology, Faculty of Veterinary Sciences, University of Extremadura, Avenida Universidad s/n, Cáceres E-10071, Spain. agmateos@unex.es
Telephone: +34-927-257000 Fax: +34-927-257110
Received: November 19, 2009
Revised: January 11, 2010
Accepted: January 18, 2010
Published online: February 6, 2010
Abstract

Alcohol abuse is a major cause of pancreatitis, a condition that can manifest as both acute necroinflammation and chronic damage (acinar atrophy and fibrosis). Pancreatic acinar cells can metabolize ethanol via the oxidative pathway, which generates acetaldehyde and involves the enzymes alcohol dehydrogenase and possibly cytochrome P4502E1. Additionally, ethanol can be metabolized via a nonoxidative pathway involving fatty acid ethyl ester synthases. Metabolism of ethanol by acinar and other pancreatic cells and the consequent generation of toxic metabolites, are postulated to play an important role in the development of alcohol-related acute and chronic pancreatic injury. This current work will review some recent advances in the knowledge about ethanol actions on the exocrine pancreas and its relationship to inflammatory disease and cancer.

Keywords: Pancreas; Calcium; Ethanol; Reactive oxygen species; Pancreatitis