Gao Z Y, Drews G, Henquin J C
Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, Brussels, Belgium.
Biochem J. 1991 May 15;276 ( Pt 1)(Pt 1):169-74. doi: 10.1042/bj2760169.
Oxytocin (OT) produced a dose-dependent increase in somatostatin, glucagon and insulin release by isolated mouse islets. A small effect on somatostatin release was observed with 0.1 nM-OT, but 1-10 nM-OT was required to affect A- and B- cells significantly. The effects of OT on somatostatin and glucagon release were similar in the presence of 3 mM- and 10 mM-glucose. No change in insulin release was produced by OT in 3 mM-glucose, but a stimulation was still observed in the presence of a maximally effective concentration of glucose (30 mM). The increase in insulin release produced by OT (in 15 mM-glucose) was accompanied by small accelerations of 86Rb and 45Ca efflux from islet cells. Omission of extracellular Ca2+ accentuated the effect of OT on 86Rb efflux, attenuated that on 45Ca efflux, and abolished that on release. OT never inhibited 86Rb efflux. It did not affect the resting potential of B-cells, but slightly increased the Ca2(+)-dependent electrical activity induced by 15 mM-glucose. OT did not affect cyclic AMP levels, but increased inositol phosphate levels in islet cells. It is suggested that the amplification of glucose-induced insulin release that OT produces is due to a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than to a change in cyclic AMP levels or a direct action on the membrane potential. Since OT is present in the pancreas, it is possible that it exerts a neuropeptidergic control of the islet function.
催产素（OT）可使分离的小鼠胰岛释放生长抑素、胰高血糖素和胰岛素呈剂量依赖性增加。0.1 nM的OT对生长抑素释放有轻微影响，但需要1 - 10 nM的OT才能显著影响A细胞和B细胞。在3 mM和10 mM葡萄糖存在的情况下，OT对生长抑素和胰高血糖素释放的影响相似。在3 mM葡萄糖条件下，OT未引起胰岛素释放变化，但在最大有效浓度葡萄糖（30 mM）存在时仍观察到刺激作用。OT（在15 mM葡萄糖中）引起的胰岛素释放增加伴随着胰岛细胞86Rb和45Ca外流的轻微加速。去除细胞外Ca2+会增强OT对86Rb外流的影响，减弱对45Ca外流的影响，并消除对释放的影响。OT从未抑制86Rb外流。它不影响B细胞的静息电位，但略微增加了由15 mM葡萄糖诱导的Ca2+依赖性电活动。OT不影响环磷酸腺苷水平，但增加了胰岛细胞中的肌醇磷酸水平。有人认为，OT产生的葡萄糖诱导的胰岛素释放放大作用是由于磷酸肌醇代谢的刺激，可能是蛋白激酶C的激活，而不是环磷酸腺苷水平的变化或对膜电位的直接作用。由于OT存在于胰腺中，它有可能对胰岛功能发挥神经肽能控制作用。
