INSULIN-SECRETION FROM PANCREATIC B-CELLS CAUSED BY L-ARGININE DERIVED NITROGEN-OXIDES
INSULIN-SECRETION FROM PANCREATIC B-CELLS CAUSED BY L-ARGININE DERIVED NITROGEN-OXIDES
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DOI：
10.1126/science.1371193
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发表时间：
1992-02-07
期刊：
影响因子：
56.9
通讯作者：
MURAD, F
中科院分区：
文献类型：
--
作者：
SCHMIDT, HHHW;WARNER, TD;MURAD, F
l -精氨酸引起胰腺B细胞释放胰岛素。来自三个模型系统的数据支持了l -精氨酸衍生的氮氧化物（NOs）介导胰岛素释放的假设，这些胰岛素释放是由l -精氨酸在d -葡萄糖和降糖药物甲苯丁胺的存在下刺激的。通过化学和NO诱导鸟苷3′，5′-单磷酸的积累，检测胰腺B细胞中NO的形成。N(G)取代的l -精氨酸类似物抑制胰岛素和NO的释放。蛋白免疫印迹和抗血清I型NO合成酶的组织化学分析表明，胰腺B细胞中NO的形成是由NADPH-（烟酰胺腺嘌呤二核苷酸磷酸的还原形式）催化的，Ca2+/钙调素依赖的I型NO合成酶约为150千dalton。
L-Arginine causes insulin release from pancreatic B cells. Data from three model systems support the hypothesis that L-arginine-derived nitrogen oxides (NOs) mediate insulin release stimulated by L-arginine in the presence of D-glucose and by the hypoglycemic drug tolbutamide. The formation of NO in pancreatic B cells was detected both chemically and by the NO-induced accumulation of guanosine 3',5'-monophosphate. N(G)-substituted L-arginine analogs inhibited the release of both insulin and NO. Protein immunoblot and histochemical analysis with antiserum to type I NO synthase suggest that the formation of NO in pancreatic B cells is catalyzed by an NADPH- (reduced form of nicotinamide adenine dinucleotide phosphate), Ca2+/calmodulin-dependent type I NO synthase of about 150 kilodaltons.