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胰腺酶对流食餐及激素刺激的反应。与血浆促胰液素和胆囊收缩素水平的相关性。

Pancreatic enzyme response to a liquid meal and to hormonal stimulation. Correlation with plasma secretin and cholecystokinin levels.

作者信息

Beglinger C, Fried M, Whitehouse I, Jansen J B, Lamers C B, Gyr K

出版信息

J Clin Invest. 1985 May;75(5):1471-6. doi: 10.1172/JCI111850.

Abstract

Pancreatic trypsin output and plasma secretin and cholecystokinin (CCK) levels were measured in five healthy volunteers to investigate the mechanisms involved in regulating postprandial pancreatic secretion. The pancreas was stimulated by a liquid test meal or by either intravenous secretin (1-82 pmol/kg-1 per h-1) or caerulein, a CCK analogue (2.3-37 pmol/kg-1 per h-1), or by a combination of secretin and caerulein. Pancreatic secretion was assessed by a marker perfusion technique (polyethylene glycol [PEG 4000]), plasma secretin, and CCK by specific radioimmunoassays. Increasing doses of secretin produced increasing bicarbonate output (P less than 0.01), whereas trypsin was not stimulated over basal. Graded caerulein produced a stepwise increase in trypsin and bicarbonate output (P less than 0.01). Potentiation occurred for bicarbonate secretion between secretin and caerulein, but not for trypsin output. Postprandial trypsin secretion averaged 29.1 IU/min-1 over 150 min (equal to 55% of maximal response to caerulein). The peak trypsin response amounted to 90% of maximal caerulein. Significant increases of plasma secretion (P less than 0.05) and CCK (P less than 0.01) were observed after the meal. Comparison of enzyme and CCK responses to the testmeal or to exogenous caerulein suggested that the amount of CCK released after the meal could account for the postprandial trypsin secretion. We conclude that (a) the postprandial enzyme response in man is submaximal in comparison to maximal exogenous hormone stimulation; (b) CCK is a major stimulatory mechanism of postprandial trypsin secretion, whereas secretin is not involved; and (c) Potentiation of enzyme secretion is not a regulatory mechanism of the postprandial secretory response.

摘要

对五名健康志愿者测量了胰腺胰蛋白酶分泌量以及血浆促胰液素和胆囊收缩素(CCK)水平,以研究参与调节餐后胰腺分泌的机制。通过液体试验餐或静脉注射促胰液素(1 - 82 pmol/kg-1每小时-1)或CCK类似物蛙皮素(2.3 - 37 pmol/kg-1每小时-1)或促胰液素与蛙皮素联合刺激胰腺。通过标记灌注技术(聚乙二醇[PEG 4000])评估胰腺分泌,通过特异性放射免疫测定法测定血浆促胰液素和CCK。促胰液素剂量增加导致碳酸氢盐分泌量增加(P < 0.01),而胰蛋白酶分泌未超过基础水平。分级给予蛙皮素使胰蛋白酶和碳酸氢盐分泌量逐步增加(P < 0.01)。促胰液素和蛙皮素之间对碳酸氢盐分泌有协同作用,但对胰蛋白酶分泌量无协同作用。餐后150分钟内胰蛋白酶分泌平均为29.1 IU/min-1(相当于对蛙皮素最大反应的55%)。胰蛋白酶反应峰值达到蛙皮素最大反应的90%。餐后观察到血浆促胰液素(P < 0.05)和CCK(P < 0.01)显著增加。酶和CCK对试验餐或外源性蛙皮素反应的比较表明,餐后释放的CCK量可解释餐后胰蛋白酶分泌。我们得出结论:(a)与最大外源性激素刺激相比,人类餐后酶反应未达到最大值;(b)CCK是餐后胰蛋白酶分泌的主要刺激机制,而促胰液素不参与;(c)酶分泌的协同作用不是餐后分泌反应的调节机制。

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