NUTRIENT INDUCED GASTRIC PROTECTION--ROLE OF CCK

营养诱导的胃保护——CCK 的作用

• 批准号: 6177475
• 负责人: DAVID W MERCER
• 金额: $ 11.16万
• 依托单位: UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-08-01 至 2001-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6177475
• 关键词: adenosinetriphosphatase; alcoholic beverage consumption; aspirin; chemoprevention; chlorine; cholanate compound; cholecystokinin; electrophysiology; enzyme activity; gastric mucosa; gastrointestinal epithelium; gastrointestinal pharmacology; gastrointestinal stimulator; hormone receptor; hormone regulation /control mechanism; ion transport; laboratory rabbit; laboratory rat; medical rehabilitation related tag; nutrient intake activity; nutrition related tag; radioactive microsphere technique; radioimmunoassay; sodium potassium exchanging ATPase; somatostatin

Cholecystokinin (CCK) is a gut peptide produced by CCK cells located in the duodenum and proximal jejunum. The major dietary intestinal stimuli for its release are intact proteins and fatty acids. Recent observations suggest that this gut peptide may serve a far more fundamental purpose than simply coordinating digestion of a meal. It has been shown that CCK is capable of maintaining gastric mucosal Integrity In the face of a damaging luminal insult. Consequently, it seems likely that nutrients contained within an Ingested meal stimulate the release of gut peptides, such as CCK, that not only coordinate the digestive process, but also promote intestinal health and render the gut more resistant to damage from luminal irritants that often accompany a meal. Gastric injury from excessive alcohol consumption or ingestion of aspirin continues to be a major cause of upper gastrointestinal bleeding. Further, gastric ulceration remains a major clinical problem. Thus, the overall HYPOTHESIS of this research proposal is that dietary intestinal nutrients elicit the release of endogenous CCK and through such release, enables the gastric epithelium to become more resistant to injury from potentially damaging luminal challenges that would otherwise occur. The precise conditions by which CCK mediates its protective effects as well as the mechanism(s) responsible for these actions remain to be fully elucidated. This being the case, the present research proposal will address the following five specific aims. The first aim will be to characterize the conditions under which exogenous CCK prevents gastric injury. The second aim will be to determine whether nutrient induced release of endogenous CCK alters the ability of the gastric epithelium to maintain its integrity in response to a damaging insult. The third aim will ascertain the role that gastric mucosal blood flow plays in nutrient induced gastric protection. The fourth aim will elucidate the effects of exogenous CCK on gastric epithelial ion transport as a potential protective mechanism. The fifth aim will examine the effects of nutrients on gastric Na+, K+ ATPase activity. The results of this research proposal will clarify the importance of nutrients in the intrinsic gastric mucosal defense system and enhance our understanding of the physiological function of the endogenous gut peptide, CCK.

胆囊收缩素（Cholecystokinin， CCK）是一种肠内肽，由位于肠内的CCK细胞产生

项目成果

Gastroprotective actions of bombesin, L-DOPA, and mild irritants: roles of prostaglandins and sensory neurons.

铃蟾肽、左旋多巴和轻度刺激物的胃保护作用：前列腺素和感觉神经元的作用。

• 发表时间: 1998
• 期刊: Surgery
• 影响因子: 3.8
• 作者: Mercer,DW;Cross,JM;Castaneda,AA;Gunter,JA
• 通讯作者: Gunter,JA

Effects of intestinal ischemia/reperfusion injury on gastric acid secretion.

肠道缺血/再灌注损伤对胃酸分泌的影响。

• DOI: 10.1006/jsre.2000.5853
• 发表时间: 2000
• 期刊: The Journal of surgical research
• 作者: Castañeda,A;Vilela,R;Chang,L;Mercer,DW
• 通讯作者: Mercer,DW

Effects of cholecystokinin on gastric injury and gastric mucosal blood flow.

胆囊收缩素对胃损伤和胃粘膜血流的影响。

• DOI: 10.1016/s1091-255x(98)80013-9
• 发表时间: 1998
• 期刊: Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
• 作者: Cross,JM;Chang,L;Mercer,DW
• 通讯作者: Mercer,DW