Liddle R A
Duke University Medical Center, Durham, North Carolina.
Gastroenterol Clin North Am. 1989 Dec;18(4):735-56.
This article has centered on the hormonal actions of CCK on a variety of different target tissues. Until the development of specific assays for measuring plasma levels of the hormone, it was not possible to distinguish physiologic from pharmacologic effects. However, by the methods described earlier it now has become clear that CCK, in physiologic concentrations, stimulates gallbladder contraction, delays gastric emptying, potentiates insulin secretion, and may affect satiety. Actions of CCK that have been studied by radioimmunoassay methods and determined also to be physiologic include stimulation of pancreatic exocrine secretion. Other actions of CCK that may be physiologic but have not been thoroughly investigated include effects on bowel motility, relaxation of lower esophageal sphincter pressure, regulation of sphincter of Oddi pressure, effects on analgesia, and modification of behavior. Some of these actions may be attributable to endogenous, but neurally released CCK and, therefore, would not be hormonal actions. However, continued investigations with specific CCK receptor antagonists together with accurate measurements of circulating levels of CCK should make it possible to define the physiologic importance of CCK on these other potential sites of action. The variety of CCK's physiologic effects emphasizes its integrative function on both digestive and metabolic processes. After a meal, in a highly coordinated fashion, CCK (1) regulates the movement of nutrients through the gastrointestinal tract, (2) contracts the gallbladder and stimulates pancreatic exocrine secretion to facilitate digestion, and (3) potentiates amino acid-induced insulin secretion and delays gastric emptying to maintain euglycemia. An effect to reduce food intake following food ingestion would be a logical extension of these integrated actions. Thus, CCK appears to have an essential role in regulating the intake, processing, and distribution of essential nutrients.
本文着重探讨了胆囊收缩素（CCK）对多种不同靶组织的激素作用。在能够测定血浆中该激素水平的特异性检测方法开发出来之前，无法区分其生理效应和药理效应。然而，通过前文所述的方法，现在已经明确，生理浓度的CCK可刺激胆囊收缩、延缓胃排空、增强胰岛素分泌，并可能影响饱腹感。通过放射免疫分析方法研究并确定为生理作用的CCK作用还包括刺激胰腺外分泌。CCK的其他可能具有生理作用但尚未得到充分研究的作用包括对肠道运动的影响、降低食管下括约肌压力、调节奥迪括约肌压力、镇痛作用以及行为改变。其中一些作用可能归因于内源性但经神经释放的CCK，因此不属于激素作用。然而，继续使用特异性CCK受体拮抗剂进行研究，并准确测量CCK的循环水平，应该能够确定CCK在这些其他潜在作用部位的生理重要性。CCK多种生理效应强调了其在消化和代谢过程中的整合功能。进食后，CCK以高度协调的方式：（1）调节营养物质在胃肠道中的移动；（2）收缩胆囊并刺激胰腺外分泌以促进消化；（3）增强氨基酸诱导的胰岛素分泌并延缓胃排空以维持血糖正常。进食后减少食物摄入量的作用将是这些整合作用的合理延伸。因此，CCK似乎在调节必需营养素的摄入、加工和分配方面起着重要作用。
