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目的明确ghrelin在离体大鼠胰岛中对胰岛素分泌和内向整流钾通道(Kir6.2)表达的影响,并讨论两者的关系。方法离体大鼠胰岛以高浓度葡萄糖及不同浓度ghrelin和(或)其受体拮抗剂[D-lys3]-GHRP-6孵育1h,采用放免法测定上清液的胰岛素,采用RT-PCR检测Kit6.2、磺酰脲受体1(SUR-1)、解偶联蛋白2(UCP-2)、葡萄糖转运子2(GluT-2)、胰十二指肠同源盒1(PDX-1)等基因的表达。结果10-8～10-6mol/L ghrelin呈剂量依赖性抑制离体大鼠胰岛高浓度葡萄糖刺激的胰岛素释放,且剂量依赖性增加Kir6.2 mRNA表达,但对SUR-1、UCP-2、GluT-2及PDX-1 mRNA表达则无显著影响。[D-lys3]-GHRP-6可消除ghrelin对Kir6.2 mRNA表达的上调作用。结论在离体大鼠胰岛中,ghrelin通过作用于其受体,促进ATP敏感性钾通道组成成分Kir6.2的表达,改变钾通道功能状态。这可能是ghrelin抑制葡萄糖刺激的胰岛素分泌的机制之一。
Objective To investigate the effect of ghrelin on insulin secretion and the expression of inward rectifier potassium channel (Kir6.2) in isolated rat islets, and discuss the relationship between them. Methods Rat islets were incubated with high concentration of glucose and ghrelin and / or its receptor antagonist [D-lys3] -GHRP-6 for 1 h. The supernatant was measured by radioimmunoassay and detected by RT-PCR Kit6.2, SUR-1, UCP-2, GluT-2, PDX-1 ) And other gene expression. Results ghrelin 10-8 ~ 10-6mol / L inhibited the release of insulin induced by glucose in a dose-dependent manner in a dose-dependent manner in a dose-dependent manner and increased the expression of Kir6.2 mRNA in a dose-dependent manner. However, the effects of SUR-1, UCP-2, GluT-2 and PDX-1 mRNA expression had no significant effect. [D-lys3] -GHRP-6 abolished the upregulation of Kir6.2 mRNA expression by ghrelin. Conclusion In isolated rat islets, ghrelin promotes the expression of Kir6.2, an ATP-sensitive potassium channel, and changes the functional status of potassium channels. This may be one of the mechanisms by which ghrelin inhibits glucose-stimulated insulin secretion.