ETHANOL AND PANCREATITIS

乙醇与胰腺炎

• 批准号: 2898791
• 负责人: Fred Sanford Gorelick
• 金额: $ 1.5万
• 依托单位: AMERICAN PANCREATIC ASSOCIATION, INC.
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-09-01 至 2000-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2898791
• 关键词: alcoholism /alcohol abuse; ethanol; meeting /conference /symposium; pancreatitis; travel

The mechanisms responsible for generating alcohol-induced pancreatitis are largely unknown. This grant proposal requests support for a multi-disciplinary workshop that will discuss alcohol-induced injury with particular emphasis on the effect of this agent on the exocrine pancreas. Ethanol toxicity may be related to both its acute and chronic effects. Further, ethanol may be directly toxic, be metabolized to, or stimulate the generation of toxic agents. One of the important features of alcoholic pancreatitis is that few abusers develop the disease. This fact suggests that important genetic or environmental factors may influence the development of the disease. The importance of these factors in the pathogenesis of alcohol-induced pancreatitis remains unclear. However, important and potentially relevant observations have been made in other systems and particularly in studies of hepatic toxicity. These include studies of receptor function, vesicular trafficking, proteolysis, and cellular energy production in hepatocytes. Studies of ethanol-induced pancreatic disease have been hampered by the lack of a suitable experimental model. However, some progress has been made in developing suitable models. Further, studies of ethanol toxicity in experimental models have identified effects of the agent that may be relevant to human disease. The findings include enhanced proteolysis within the acinar cell in response to cholecystokinin and ethanol sensitization of rats in the cerulein model of pancreatitis. The non-oxidative ethanol metabolite, non-esterified free fatty acid, may also sensitize the pancreas to injurious stimulation. The aims of the meeting are to bring together investigators interested in the toxic effects of ethanol in either the pancreas or other systems and present information that may be useful for studies of pancreatic diseases. Investigators in the pancreatic field will present cutting edge studies that include such topics as new models of ethanol-induced pancreatic damage and the effects of ethanol on gene transcription. The format of the meeting will be a combination of 30 min overviews, 15 min presentations of original data, and State of the Art Lectures. Young investigators will be invited to participate in the meeting and to present posters on this topic. Support for young investigators expenses will be sought from the American Gastroenterological Association Research Committee. The meeting Will last for one and a half days and immediately follow the annual meeting of the American Pancreatic Association in Chicago, IL, Nov. 5 to Nov. 7, 1999.

造成酒精诱发胰腺炎的机制在很大程度上尚不清楚。 该拨款提案请求支持一个多学科研讨会，该研讨会将讨论酒精引起的损伤，特别强调该药物对外分泌胰腺的影响。 乙醇毒性可能与其急性和慢性影响有关。 此外，乙醇可能具有直接毒性、被代谢成有毒物质或刺激有毒物质的产生。 酒精性胰腺炎的重要特征之一是很少有滥用者患上这种疾病。这一事实表明重要的遗传或​​环境因素可能会影响疾病的发展。 这些因素在酒精性胰腺炎发病机制中的重要性仍不清楚。 然而，在其他系统中，特别是在肝毒性研究中，已经进行了重要且可能相关的观察。 这些包括肝细胞中受体功能、囊泡运输、蛋白水解和细胞能量产生的研究。由于缺乏合适的实验模型，乙醇诱发的胰腺疾病的研究受到阻碍。 然而，在开发合适的模型方面已经取得了一些进展。 此外，在实验模型中对乙醇毒性的研究已经确定了该物质可能与人类疾病相关的作用。 研究结果包括，在雨蛙素胰腺炎模型中，大鼠腺泡细胞内的蛋白水解作用增强，以响应胆囊收缩素和乙醇致敏作用。 非氧化性乙醇代谢物、非酯化游离脂肪酸也可能使胰腺对有害刺激敏感。 会议的目的是聚集对乙醇对胰腺或其他系统的毒性作用感兴趣的研究人员，并提供可能对胰腺疾病研究有用的信息。 胰腺领域的研究人员将展示前沿研究，其中包括乙醇引起的胰腺损伤的新模型以及乙醇对基因转录的影响等主题。 会议的形式将包括 30 分钟的概述、15 分钟的原始数据演示和最新技术讲座。年轻的研究人员将被邀请参加会议并展示有关该主题的海报。 年轻研究人员的费用将寻求美国胃肠病学协会研究委员会的支持。 会议将持续一天半，紧接着于1999年11月5日至7日在伊利诺伊州芝加哥举行的美国胰腺协会年会。