INTEGRATED ROLE OF CCK ON THE GASTROINTESTINAL TRACT
INTEGRATED ROLE OF CCK ON THE GASTROINTESTINAL TRACT
批准号:
3238045
负责人:
Rodger A. Liddle
金额:
$15.4万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1988
资助国家:
美国
项目状态:
已结题
起止时间:
1988-07-14 至 1991-06-30
关键词:
adrenergic receptor bombesin chemical structure function cholecystokinin cholelithiasis diabetes mellitus dopamine receptor gallbladder gastrointestinal system genetic transcription glucose tolerance test hormone biosynthesis hormone metabolism hormone regulation /control mechanism human subject insulin laboratory rat messenger RNA muscarinic receptor neurohormones neuropeptide receptor neurotransmitters obesity peptide analog somatostatin stomach emptying
中文摘要
虽然CCK是一种有效的胃肠激素,但很少有
了解它的生理学和病理学。随着最近的
灵敏、特异的空腹检测方法的研制
以及餐后血浆CCK水平,这是CCK的主要刺激因素
CCK在靶组织中的分泌和生理作用
现在要下定决心。这项拟议的研究将研究
神经递质和激素对CCK分泌的调节
CCK对靶组织的作用。CCK的分泌将是
CCK对胃排空、胆汁分泌的影响
正常人和患者的膀胱收缩和胰岛素释放
患有各种疾病。头位刺激CCK分泌,
将对胃肠的作用机制进行研究和调控
将评估神经激素制剂释放CCK的情况。在……里面
肥胖,CCK对胃排空改变的贡献,
胆汁收缩、胆结石形成和葡萄糖
新陈代谢也将被研究。CCK的分泌和分泌
胆结石患者的胆囊收缩是正常的
将对疾病进行调查。由于CCK增强了胰岛素
分泌,CCK对胰岛素分泌和血糖的作用
耐受性将在正常受试者和患有
非胰岛素依赖型糖尿病。
在大鼠模型中CCK的饮食和药物调节
分泌和CCK的合成将被研究。的影响
胆碱能、肾上腺素能和多巴胺能因子以及
胃肠激素蛙皮素、生长抑素和PYY对CCK的影响
释放将会被确定。CCK分泌与血管紧张素转换酶的关系
肠道CCK的生物合成将通过测量来评估
血浆CCK、肠道CCK含量及CCK mRNA水平。
这些在人类和大鼠身上的研究应该会提供对
CCK在健康和疾病中的作用。
英文摘要
Although cholecystokinin (CCK) is a potent GI hormone, little is
know about its physiology and pathology. With the recent
development of sensitive and specific assays for measuring fasting
and postprandial plasma levels of CCK, the major stimuli for CCK
secretion and the physiologic role of CCK in target tissues can
now be determined. This proposed research will study the
regulation of CCK secretion by neurotransmitters and hormones
and the action of CCK on target tissues. CCK secretion will be
correlated with the actions of CCK on gastric emptying, gall
bladder contraction, and insulin release in normals and patients
with various diseases. Stimulation of CCK secretion by cephalic,
gastric, and intestinal mechanisms will be studied and regulation
of CCK release by neurohormonal agents will be evaluated. In
obesity, the contribution of CCK to altered gasteric emptying,
gall bladder contraction, gallstone development, and glucose
metabolism will also be studied. Whether CCK secretion and
gallbladder contraction are normal in patients with gallstone
disease will be investigated. Since CCK potentiates insulin
secretion, the role of CCK on insulin secretion and glucose
tolerance will be evaluated in normal subjects and in patients with
non-insulin dependent diabetes mellitus.
In rat models, the dietary and pharmacologic regulation of CCK
secretion and CCK synthesis will be studied. The effects of
cholinergic, adrenergic, and dopaminergic factors as well as those
of the gut hormones bombesin, somatostatin and PYY on CCK
release will be determined. The relationship of CCK secretion to
intestinal CCK biosynthesis will be evaluated by measuring
plasma CCK, intestinal CCK content and CCK mRNA levels.
These studies in humans and rats should provide insight into the
role of CCK in health and diseases.
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