乙醇消费作为胰腺炎的诱因。
Ethanol consumption as inductor of pancreatitis.
作者信息
Tapia José A, Salido Ginés M, González Antonio
机构信息
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.
出版信息
World J Gastrointest Pharmacol Ther. 2010 Feb 6;1(1):3-8. doi: 10.4292/wjgpt.v1.i1.3.
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.
酒精滥用是胰腺炎的主要病因，胰腺炎可表现为急性坏死性炎症和慢性损伤（腺泡萎缩和纤维化）。胰腺腺泡细胞可通过氧化途径代谢乙醇，该途径产生乙醛，涉及乙醇脱氢酶，可能还涉及细胞色素P4502E1。此外，乙醇可通过涉及脂肪酸乙酯合酶的非氧化途径代谢。腺泡细胞和胰腺其他细胞对乙醇的代谢以及由此产生的有毒代谢产物，被认为在酒精相关的急性和慢性胰腺损伤的发生中起重要作用。本研究将综述乙醇对外分泌胰腺作用及其与炎症性疾病和癌症关系的相关知识的一些最新进展。
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