Tsumura Y, Kagawa S, Yoshida K, Kobayashi K, Matsuoka A
Endocrinol Jpn. 1979 Dec;26(6):637-48. doi: 10.1507/endocrj1954.26.637.
To clarify the insulin-releasing mechanism, we studied insulin release and the efflux of [32P]phosphate by glucose at 0.1 mM/min of gradient level or at 16.7 mM, and other metabolism in islets of rat Langerhans. When treated with 1 mM iodoacetic acid (IAA) plus the anomers of D-glucose at 2.8 mM for 6 min at 37 degrees C, islets elicited insulin at half the control rate under the step-wise stimulation by glucose and at the same rate as the control under the slow-rise stimulation by glucose. Using islets treated with IAA plus the alpha anomer at 16.7 mM, the step-wise stimulation secreted insulin at half a rate of the control and the slow-rise stimulation at the rate lower than the control, which was not significantly different from the control rate. Treatment with IAA plus the beta anomer at 16.7 mM inhibited insulin release under both types of stimulations by glucose. The step-wise stimulation caused the same rapid efflux of [32P]phosphate from IAA-treated islets as from the control islets, except for islets treated with IAA plus the beta anomer at 16.7 mM. The rate of glucose utilization in islets was inhibited by all IAA-treatments to the same extent, being merely half the control rate. Treatments with IAA plus the anomers at 16.7 mM significantly reduced the formation of [3H]-cAMP and the activity of protein phosphokinase in islets, while in the presence of the anomers at 2.8 mM IAA produced no significant effect. Neither IAA-treatments altered the uptake of 45Ca and the ATP content in islets. The uptake of [14C]IAA was significantly enhanced by the presence of the beta anomer at 16.7 mM to two times the control level. On the basis of these results, we suggested that the B cell might contain both glucoreceptors and rate-sensors of glucose controlling insulin release and the former might be less sensitive to IAA as compared with the latter.
为阐明胰岛素释放机制，我们研究了大鼠胰岛中胰岛素的释放以及在0.1 mM/分钟的梯度水平或16.7 mM葡萄糖作用下[32P]磷酸盐的流出，以及其他代谢情况。当在37℃下用1 mM碘乙酸（IAA）加2.8 mM的D-葡萄糖异头物处理6分钟时，胰岛在葡萄糖逐步刺激下的胰岛素分泌速率为对照速率的一半，而在葡萄糖缓慢升高刺激下的分泌速率与对照相同。使用用IAA加16.7 mM的α异头物处理的胰岛，逐步刺激下胰岛素分泌速率为对照的一半，缓慢升高刺激下的分泌速率低于对照，但与对照速率无显著差异。用IAA加16.7 mM的β异头物处理可抑制葡萄糖两种刺激类型下的胰岛素释放。除了用IAA加16.7 mM的β异头物处理的胰岛外，逐步刺激导致IAA处理的胰岛中[32P]磷酸盐的流出速度与对照胰岛相同。所有IAA处理均同等程度地抑制胰岛中的葡萄糖利用率，仅为对照速率的一半。用IAA加16.7 mM的异头物处理显著降低了胰岛中[3H]-cAMP的形成和蛋白磷酸激酶的活性，而在2.8 mM异头物存在下IAA无显著影响。IAA处理均未改变胰岛中45Ca的摄取和ATP含量。16.7 mM的β异头物存在显著增强了[14C]IAA的摄取，使其达到对照水平的两倍。基于这些结果，我们认为B细胞可能同时含有控制胰岛素释放的葡萄糖受体和葡萄糖速率传感器，并且前者对IAA的敏感性可能低于后者。
