Potau N, Mössner J, Williams J A, Goldfine I D
Biochem Biophys Res Commun. 1984 Feb 29;119(1):359-64. doi: 10.1016/0006-291x(84)91659-0.
The binding of 125I-labeled insulin-like growth factor II (125I-IGF II) to mouse pancreatic acini was stimulated (45%) by insulin and inhibited (30%) by cholecystokinin octapeptide (CCK8). When CCK8 and insulin were added together, the effect on IGF II binding was similar to that seen when CCK8 was added alone. Two lines of evidence suggest that this effect of cholecystokinin on basal and insulin-stimulated 125I-IGF II binding was mediated via a change in intracellular calcium: (1) the cholinergic agent carbachol inhibited IGF II binding to its receptors; (2) addition of the Ca2+ ionophore A23187 mimicked the effects of CCK8 and carbachol. In contrast to its effects on IGF II binding to acini, CCK8 had only small effects on IGF I binding and no effects on insulin binding.
125I标记的胰岛素样生长因子II(125I-IGF II)与小鼠胰腺腺泡的结合受到胰岛素刺激(增加45%),并受到八肽胆囊收缩素(CCK8)抑制(减少30%)。当CCK8和胰岛素同时添加时,对IGF II结合的影响与单独添加CCK8时相似。有两条证据表明,胆囊收缩素对基础状态及胰岛素刺激的125I-IGF II结合的这种作用是通过细胞内钙的变化介导的:(1)胆碱能药物卡巴胆碱抑制IGF II与其受体的结合;(2)添加Ca2+离子载体A23187可模拟CCK8和卡巴胆碱的作用。与对IGF II与腺泡结合的影响相反,CCK8对IGF I结合的影响很小,对胰岛素结合则无影响。