IKdelay is related to a novel GLP-1 pathway that is KATP-independent insulin secretion.

胰岛β细胞的IKdelay在葡萄糖刺激的胰岛素分泌中起重要作用。延迟电流在葡萄糖刺激产生动作电位时是活跃的。当葡萄糖浓度从2.8mM增加到16.7mM时，IKdelay的振幅增加。这些增加仅在正电位处观察到，伴随着负电位范围内的电流减少。相反，在细胞质上使用FCCP、AMPPNP或0mM ATP暴露，葡萄糖减少或代谢抑制产生的IKdelay在负电位下增加，而在正电位下电流减少。我们进一步在代谢抑制过程中表达Kv2.1通道的HEK293细胞中观察到类似的结果。在Kv2.1通道表达的HEK293细胞中，细胞质暴露于碱性磷酸酶后，电流呈负电位增加。因此，胰腺β细胞在代谢抑制过程中观察到的IKdelay变化是由Kv2.1通道的去磷酸化引起的，因为该通道蛋白具有在基础状态下可高度磷酸化的氨基酸残基。我们得出结论，Kv2.1通道电流受通道磷酸化/去磷酸化的调节。这些结果可能表明，Kv2.1通道调节参与GLP-1效应，这种效应在激素存在时随着胰岛素分泌的增加而显现。

IKdelay in pancreatic β-cells plays important roles in glucose-stimulated insulin secretion. IKdelay current is active during action potentials produced by glucose stimulation. Amplitudes of IKdelay are increased by increasing glucose concentrations from 2.8mM to 16.7mM. These increases were observed only at positive potentials were accompanied by the current decreases in the ranges of negative potentials. Conversely glucose reduction or metabolic inhibition by using FCCP, AMPPNP or 0mM ATP exposure at cytoplasm produced IKdelay increases at negative potentials associated with current decreases at positive potentials. We further observed the similar results in the HEK293 cells expressed with Kv2.1 channels during metabolic inhibition. Exposure to alkaline phosphatase at the cytoplasm showed current increases at negative potentials in Kv2.1 channel-expressed HEK293 cells. Thus, IKdelay changes observed in pancreatic β-cells during metabolic inhibition were resulted from the dephosphorylation of Kv2.1 channels because the channel protein has amino acid residues that can be highly phosphorylated at basal state. We concluded that Kv2.1 channel current is regulated by phosphorylation/dephosphorylation of the channel. These results may suggest that Kv2.1 channel regulation is involved in GLP-1 effect that is revealed with increases insulin secretion in the presence of the hormone.