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:
影响因子:
--
通讯作者:
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
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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DOI:
10.1056/nejm197306072882302
发表时间:
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期刊:
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