Open AccessEthanol consumption as inductor of pancreatitis
Author(s) -
José A. Tapia,
Ginés M. Salido,
Antonio González
Publication year - 2010
Publication title -
world journal of gastrointestinal pharmacology and therapeutics
Language(s) - English
Resource type - Journals
ISSN - 2150-5349
DOI - 10.4292/wjgpt.v1.i1.3
Subject(s) - pancreatitis , acetaldehyde , medicine , cyp2e1 , alcohol dehydrogenase , pancreas , ethanol metabolism , ethanol , pancreatic cancer , atrophy , acute pancreatitis , pancreatic disease , pancreatic injury , fibrosis , cytochrome p450 , pharmacology , endocrinology , chemistry , biochemistry , metabolism , cancer
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.