Mediation of insulin release by cGMP and cAMP in a starved animal model.
Mediation of insulin release by cGMP and cAMP in a starved animal model.
复制标题
在饥饿动物模型中，cGMP 和 cAMP 介导胰岛素释放。
DOI：
10.1016/0303-7207(83)90079-5
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发表时间：
1983
影响因子：
4.1
通讯作者：
Laychock,SG
中科院分区：
文献类型：
--
作者：
Laychock,SG
从进食大鼠分离的胰岛响应于葡萄糖、8-溴鸟苷3 '，5'-环一磷酸（8-Br-cGMP）和8-溴腺苷3 '，5'-环一磷酸（8-Br-cAMP）而释放胰岛素，但不响应于8-溴肌苷3 '，5'-环一磷酸。饥饿大鼠48小时显着减少胰岛素释放的胰岛在这些代理商，降低内源性cGMP和cAMP水平。cGMP和cAMP的类似物增强葡萄糖反应的剂量依赖性的方式在胰岛从饥饿的大鼠，而在喂养的大鼠胰岛的环核苷酸类似物没有增强葡萄糖刺激的胰岛素释放。硝普钠可提高胰岛内源性cGMP水平，也可增强饥饿大鼠胰岛的葡萄糖反应。甘露庚酮糖抑制葡萄糖和8-Br-cGMP刺激的胰岛素释放，但不抑制8-Br-cAMP刺激的胰岛素释放。这些结果表明，从饥饿动物的胰岛受损的葡萄糖反应部分是由于减少的环核苷酸水平，和cGMP在胰岛素分泌中的作用可能包括葡萄糖代谢的增强。
Islets isolated from fed rats released insulin in response to glucose, 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP) and 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP), but not to 8-bromoinosine 3',5'-cyclic monophosphate. Starving rats for 48 h significantly diminished insulin release from islets in response to these agents, and lowered endogenous levels of cGMP and cAMP. The analogs of cGMP and cAMP potentiated the glucose response in a dose-dependent manner in islets from starved rats, whereas in fed rat islets the cyclic nucleotide analogs did not potentiate glucose-stimulated insulin release. Sodium nitroprusside, which enhances endogenous cGMP levels in islets, also enhanced the glucose response in islets from starved rats. Mannoheptulose inhibited glucose and 8-Br-cGMP-stimulated insulin release, but not 8-Br-cAMP-stimulated release. These results suggest that the impaired glucose response of islets from starved animals is in part due to diminished levels of cyclic nucleotides, and that the role(s) of cGMP in insulin secretion may include enhancement of glucose metabolism.