CHOLECYSTIKININ SECRETION & ACTION IN PATIENT WITH INSULIN RESISTANCE

缩胆囊素(CCK)，一种从 喂食过程中的肠道，刺激胰腺外分泌 分泌物、胆囊壁收缩和肠道运动。因为 在以前测量CCK水平的困难中，几乎没有 知道荷尔蒙的生理学和病理学。这个 首席调查员最近开发了一种敏感的和 测定空腹和餐后的特异性生物测定法 血浆CCK水平并已证明生理性 CCK浓度通过以下途径直接调节β细胞功能 增强氨基酸诱导的胰岛素分泌。此外，他的 非胰岛素依赖型糖尿病患者的初步研究 糖尿病(NIDDM)表现为CCK分泌异常 喂食混合流质的食物。 这项拟议的研究将考察CCK在受损人群中的作用 从四个方面研究NIDDM的胰岛素分泌 项目1.CCK中描述的患者及其家属群体 将在：(1)非糖尿病受试者中研究分泌和作用 有相对胰岛素敏感性，(2)非糖尿病患者有 相对胰岛素抵抗，(3)胰岛素抵抗和 糖耐量异常；(4)NIDDM患者。会是 确定任一种CCK分泌是否存在异常， 慢性阻塞性肺疾病患者对CCK作用的β细胞抵抗 胰岛素分泌受损以及这种缺陷是否会 由CCK管理部门更正。最后，它将是 确定是否有CCK分泌的家族模式或 导致异常分泌的行为。

Cholecystokinin (CCK), a polypeptide hormone that is released from the intestine during feeding, stimulates pancreatic exocrine secretion, gallbladder contraction, and bowel motility. Because of prior difficulties in measuring blood levels of CCK, little is known about the physiology and pathology of the hormone. The principal investigator has recently developed a sensitive and specific bioassay for measuring both fasting and postprandial plasma levels of CCK and has demonstrated that physiological concentrations of CCK directly regulate beta cell function by potentiating amino acid-induced insulin secretion. Moreover, his preliminary studies in patients with non-insulin dependent diabetes mellitus (NIDDM) demonstrate abnormal CCK secretion in response to feeding a mixed liquid meal. The proposed research will examine the role of CCK in the impaired insulin secretion of NIDDM by investigating four well characterized groups of patients and their families described in Project 1. CCK secretion and action will be studied in: (1) non-diabetic subjects with relative insulin sensitivity, (2) non-diabetic subjects with relative insulin resistance, (3) those with insulin resistance and abnormal glucose tolerance, and (4) those with NIDDM. It will be determined whether there is an abnormality in either CCK secretion, or beta cell resistance to the actions of CCK in patients with impaired insulin secretion and whether such a defect can be corrected by the administration of CCK. Finally, it will be determined whether there are familial patterns of CCK secretion or action that contribute to abnormal secretion.