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阿片类物质对犬进食后胰多肽释放的调节作用。

Opiate modulation of pancreatic polypeptide release by a meal in the dog.

作者信息

Materia A, Modlin I M, Sank A C, Albert D, Jaffe B M

出版信息

J Pharmacol Exp Ther. 1982 Nov;223(2):355-8.

PMID:7131290
Abstract

It has been reported that morphine abolished the plasma pancreatic polypeptide (PP) response to a meal in man, but the mechanism of this action is unclear. This study was designed to investigate the effect of low doses of the endogenous opiate peptide. Met-enkephalin and naloxone on basal- and meal-stimulated PP release in order to examine the role of opioid modulation in the release of this hormone. Four gastric fistula dogs underwent a series of six studies, a test meal alone. Met-enkephalin infusion (40 microgram/kg/hr), naloxone infusion, meal plus naloxone infusion and meal plus Met-enkephalin plus naloxone. Gastrin and PP were measured by radioimmunoassay. Basal PP levels averaged 35.1 +/- 3.0 fmol/ml. Although Met-enkephalin had no effect on basal PP levels, it significantly (P less than 0.05) inhibited the mean peak increment of PP stimulated by a meal (control, 331 +/- 39 fmol/ml; Met-enkephalin, 145 +/- 49 fmol/ml; P less than 0.05). This inhibition was completely abolished by naloxone. Naloxone alone did not alter basal- or meal-stimulated plasma PP levels. Neither Met-enkephalin nor naloxone altered basal or stimulated plasma gastrin levels. This study demonstrated that opiate peptides play a role in the regulation of the release of PP by a meal; it thus suggests the possibility of an opioid modulatory mechanism for the release of this hormone.

摘要

据报道,吗啡可消除人体进食后血浆中胰多肽(PP)的反应,但其作用机制尚不清楚。本研究旨在探讨低剂量内源性阿片肽、甲硫氨酸脑啡肽和纳洛酮对基础及进食刺激的PP释放的影响,以研究阿片类物质调节在该激素释放中的作用。四只胃瘘犬进行了一系列六项研究,分别为单独的试餐、甲硫氨酸脑啡肽输注(40微克/千克/小时)、纳洛酮输注、试餐加纳洛酮输注以及试餐加甲硫氨酸脑啡肽加纳洛酮。采用放射免疫分析法测定胃泌素和PP。基础PP水平平均为35.1±3.0飞摩尔/毫升。尽管甲硫氨酸脑啡肽对基础PP水平无影响,但它显著(P<0.05)抑制了进食刺激引起的PP平均峰值增加(对照组,331±39飞摩尔/毫升;甲硫氨酸脑啡肽组,145±49飞摩尔/毫升;P<0.05)。纳洛酮可完全消除这种抑制作用。单独使用纳洛酮不会改变基础或进食刺激的血浆PP水平。甲硫氨酸脑啡肽和纳洛酮均未改变基础或刺激后的血浆胃泌素水平。本研究表明,阿片肽在进食调节PP释放中起作用;因此提示了该激素释放存在阿片类调节机制的可能性。

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