Pederson R A, Brown J C
Endocrinology. 1978 Aug;103(2):610-5. doi: 10.1210/endo-103-2-610.
Gastric inhibitory polypeptide (GIP) produced an increase in immunoreactive insulin (IRI) and immunoreactive glucagon (IRG) release from the isolated perfused rat pancreas. The magnitude of both effects was shown to be dependent on the prevailing glucose concentration. GIP stimulated IRG release at glucose concentrations less than 5.5 mM and IRI release at glucose levels greater than 5.5 mM. Arginine"stimulated IRG secretion in the presence of low glucose (2.7 mM) was potentiated by GIP. In contrast, GIP augmented arginine-stimulated insulin release only in the presence of arginine concentrations of (less than 20 mM, producing no further increase over a maximal arginine stimulus. The glucagonotropic effect of GIP in the presence of arginine was found to be suppressed by glucose, with the opposite effect observed with insulin release. It was concluded that the endocrine pancreatic action of GIP depends to a great degree on existing levels of modulating nutrients in the blood.
胃抑制多肽（GIP）可使离体灌注的大鼠胰腺释放的免疫反应性胰岛素（IRI）和免疫反应性胰高血糖素（IRG）增加。这两种效应的程度均显示取决于当时的葡萄糖浓度。GIP在葡萄糖浓度低于5.5 mM时刺激IRG释放，在葡萄糖水平高于5.5 mM时刺激IRI释放。在低葡萄糖（2.7 mM）存在的情况下，精氨酸刺激的IRG分泌被GIP增强。相反，GIP仅在精氨酸浓度低于20 mM时增强精氨酸刺激的胰岛素释放，在最大精氨酸刺激之上不会产生进一步增加。发现在精氨酸存在的情况下，GIP的促胰高血糖素作用被葡萄糖抑制，而胰岛素释放则观察到相反的效果。得出的结论是，GIP的内分泌胰腺作用在很大程度上取决于血液中调节营养物质的现有水平。
