Mechanisms of Alcoholic Pancreatitis: Introduction and Summary of the Symposium
Mechanisms of Alcoholic Pancreatitis: Introduction and Summary of the Symposium
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酒精性胰腺炎的发病机制：研讨会介绍与总结
DOI：
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Ricardo A. Brown
中科院分区：
文献类型：
--
作者：
V. Purohit;D. Russo;Marvin Salin;Ricardo A. Brown
长期大量饮酒与急性和慢性胰腺炎有关。胰腺炎的进展可能导致多种合并症，包括消化不良、糖尿病和胰腺癌。了解酒精摄入导致胰腺炎发展的潜在分子、生化和细胞机制可能有助于制定治疗和预防该疾病的策略。2002年11月，在伊利诺伊州芝加哥举行的美国胰腺协会年会上，国家酒精滥用和酒精中毒研究所和国立卫生研究院罕见疾病办公室主办了一次关于“酒精性胰腺炎机制”的卫星研讨会。本次研讨会邀请了8位发言人来讨论以下问题：(1)酒精性胰腺炎的流行病学；(2)酒精性胰腺炎的病理生理；(3)酒精性胰腺炎动物模型——胆囊收缩素（CCK）与病毒感染的关系；(4)酒精和酶原在胰腺腺泡细胞中的激活；(5)酒精代谢在酒精性胰腺炎中的作用；(6)酒精性胰腺炎的胰腺星状细胞活化；(7)酒精性慢性胰腺炎的遗传易感性。结论是，酒精滥用是急性和慢性胰腺炎发展的一个主要因素。乙醇对胰腺的损伤作用可能是通过以下途径介导的：(1)使腺泡细胞对cck诱导的酶原过早激活敏感；(2) CCK对转录因子、核因子&kgr激活的增强作用；B （NF-&kgr；B）和活化蛋白1 (AP-1)；(3)产生乙醛、脂肪酸乙酯等有毒代谢物；(4)胰腺对柯萨奇病毒B3毒性作用的致敏；(5)乙醛和氧化应激激活胰腺星状细胞，随后增加胶原蛋白和其他基质蛋白的产生。
Long-term, heavy alcohol consumption is associated with both acute and chronic pancreatitis. Progression of pancreatitis may lead to multiple comorbidities including maldigestion, diabetes, and pancreatic cancer. Understanding the underlying molecular, biochemical, and cellular mechanisms by which alcohol ingestion leads to the development of pancreatitis may help to develop strategies for the treatment and prevention of the disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Rare Diseases of National Institutes of Health sponsored a satellite symposium on “Mechanisms of Alcoholic Pancreatitis” at the annual meeting of the American Pancreatic Association, Chicago, IL, November 2002. For this symposium, 8 speakers were invited to address the following issues: (1) epidemiology of alcoholic pancreatitis; (2) pathophysiology of alcoholic pancreatitis; (3) animal models of alcoholic pancreatitis—roles of cholecystokinin (CCK) and viral infections; (4) alcohol and zymogen activation in the pancreatic acinar cell; (5) role of alcohol metabolism in alcoholic pancreatitis; (6) pancreatic stellate cell activation in alcoholic pancreatitis; and (7) genetic predisposition to alcoholic chronic pancreatitis. It was concluded that alcohol abuse is a major contributory factor to the development of both acute and chronic pancreatitis. The injurious effects of ethanol on the pancreas may be mediated through (1) sensitization of acinar cells to CCK-induced premature activation of zymogens; (2) potentiation of the effect of CCK on the activation of transcription factors, nuclear factor &kgr;B (NF-&kgr;B) and activating protein-1 (AP-1); (3) generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters; (4) sensitization of the pancreas to the toxic effects of coxsackievirus B3; and (5) activation of pancreatic stellate cells by acetaldehyde and oxidative stress and subsequent increased production of collagen and other matrix proteins.
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DOI：
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期刊：
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影响因子：
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