Carbachol modulates GIP-mediated insulin release from rat pancreatic lobules in vitro.

Carbachol modulates GIP-mediated insulin release from rat pancreatic lobules in vitro.
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Carbachol 在体外调节大鼠胰小叶 GIP 介导的胰岛素释放。

DOI:
10.1152/ajpendo.1985.248.3.e299
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发表时间:
1985
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Kalhan,SC
Kalhan,SC
中科院分区:
--
文献类型:
--
作者:
McCullough,AJ;Marshall,JB;Bingham,CP;Rice,BL;Manning,LD;Kalhan,SC

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用大鼠胰腺小叶研究了抑胃多肽(GIP)、卡巴胆碱、葡萄糖和氨基酸混合物对胰岛素分泌的相互作用。在5 mM葡萄糖下,GIP(1.1 ng/ml)在存在或不存在卡巴胆碱(5 × 10(-5)M)的情况下,在210分钟孵育期间均不增加胰岛素分泌。然而,在11 mM葡萄糖下,GIP确实增加了胰岛素分泌(342.5 +/- 62.0对212.5 +/- 50.5 microU。ml-1。mg组织-1,平均值+/- SE; P <0.01),但不存在(217.0 +/- 45.5 vs. 205.8 +/- 35.0 microU)。ml-1。mg组织-1)卡巴胆碱。在随后的30分钟孵育过程中,GIP增加至11 ng/ml的超生理浓度,并再次增加胰岛素分泌(65.8 +/- 10.8对27.8 +/- 2.4 microU)。ml-1。mg组织-1。h-1; P小于0.001),但并非没有(37.2 +/- 1.8 vs. 30.2 +/- 2 microU . ml-1。mg-1组织-1。h-1)卡巴胆碱存在。这种GIP介导的胰岛素分泌被阿托品阻断(34.8至1.8对37.6 +/- 1.6 microU。ml-1。mg组织-1。h-1)。在氨基酸浓度为21和211 mM,但不是2.1 mM时,GIP增加胰岛素释放,但再次仅与卡巴胆碱存在。总之,猪GIP在体外增加氨基酸以及葡萄糖介导的胰岛素分泌。此外,这种生物学作用依赖于一种尚未确定的胆碱能机制。神经激素相互作用的病理生理意义值得进一步研究。
Rat pancreatic lobules were used to investigate the interaction of gastric inhibitory polypeptide (GIP), carbachol, glucose, and an amino acid mixture on insulin secretion. At 5 mM glucose, GIP (1.1 ng/ml) did not augment insulin secretion in the presence or absence of carbachol (5 X 10(-5)M) during a 210-min incubation. However, at 11 mM glucose, GIP did augment insulin secretion in the presence (342.5 +/- 62.0 vs. 212.5 +/- 50.5 microU . ml-1 . mg tissue-1, mean +/- SE; P less than 0.01) but not the absence (217.0 +/- 45.5 vs. 205.8 +/- 35.0 microU . ml-1 . mg tissue-1) of carbachol. During subsequent 30-min incubations, GIP was increased to a supra-physiological concentration of 11 ng/ml and again augmented insulin secretion with (65.8 +/- 10.8 vs. 27.8 +/- 2.4 microU . ml-1 . mg tissue-1 . h-1; P less than 0.001) but not without (37.2 +/- 1.8 vs. 30.2 +/- 2 microU . ml-1 . mg-1 tissue-1 . h-1) carbachol present. This GIP-mediated insulin secretion was blocked by atropine (34.8 to 1.8 vs. 37.6 +/- 1.6 microU . ml-1 . mg tissue-1 . h-1). At amino acid concentrations of 21 and 211 mM, but not 2.1 mM, GIP augmented insulin release but again only with carbachol present. In conclusion, porcine GIP augments amino acid as well as glucose-mediated insulin secretion in vitro. Furthermore, this biological action is dependent on an, as yet, unidentified cholinergic mechanism. The pathophysiological significance of the neural-hormonal interaction deserves further investigation.
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