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首页> 外文期刊>Biology Open >Different functional roles for K+ channel subtypes in regulating small intestinal glucose and ion transport
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Different functional roles for K+ channel subtypes in regulating small intestinal glucose and ion transport

机译：K +通道亚型在调节小肠葡萄糖和离子转运中的不同功能作用

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Although K+channels are important in mediating the driving force for colonic ion transport, their role in small intestinal transport is poorly understood. To investigate this, small intestinal short circuit currents (Isc) and HCO3?secretion were measured in mice, and intracellular pH (pHi) was measured in small intestinal epithelial SCBN cells. The expression and location of Kv subtypes were verified by RT-PCR, western blotting and immunohistochemistry. Diabetic mice were also used to investigate the role of Kv subtypes in regulating intestinal glucose absorption. We found that KV7.1 is not involved in duodenal ion transport, while KCa3.1 selectively regulates duodenalIscand HCO3?secretion in a Ca2+-mediated but not cAMP-mediated manner. Blockade of KCa3.1 increased the rate of HCO3?fluxes via cystic fibrosis transmembrane conductance regulator (CFTR) channels in SCBN cells. JejunalIscwas significantly stimulated by glucose, but markedly inhibited by 4-aminopyridine (4-AP) and tetraethylammonium (TEA). Moreover, both Kv1.1 and Kv1.3 were expressed in jejunal mucosae. Finally, 4-AP significantly attenuated weight gain of normal and diabetic mice, and both 4-AP and TEA significantly lowered blood glucose of diabetic mice. This study not only examines the contribution of various K+channel subtypes to small intestinal epithelial ion transport and glucose absorption, but also proposes a novel concept for developing specific K+channel blockers to reduce weight gain and lower blood glucose in diabetes mellitus.
机译：尽管K +通道在介导结肠离子运输的驱动力方面很重要，但人们对其在小肠运输中的作用了解甚少。为了对此进行研究，在小鼠中测量小肠短路电流（Isc）和HCO3？分泌，并在小肠上皮SCBN细胞中测量细胞内pH（pHi）。通过RT-PCR，western blotting和免疫组织化学验证Kv亚型的表达和位置。糖尿病小鼠也用于研究Kv亚型在调节肠道葡萄糖吸收中的作用。我们发现，KV7.1不参与十二指肠离子的转运，而KCa3.1则以Ca2 +介导而不是cAMP介导的方式选择性地调节十二指肠Iscaned HCO3？的分泌。 KCa3.1的阻断通过SCBN细胞中的囊性纤维化跨膜电导调节剂（CFTR）通道增加了HCO3的通量。空肠Isc受到葡萄糖的明显刺激，但被4-氨基吡啶（4-AP）和四乙铵（TEA）明显抑制。此外，Kv1.1和Kv1.3均在空肠黏膜中表达。最后，4-AP显​​着减弱正常小鼠和糖尿病小鼠的体重增加，并且4-AP和TEA均显着降低糖尿病小鼠的血糖。这项研究不仅研究了各种K +通道亚型对小肠上皮离子运输和葡萄糖吸收的贡献，而且提出了开发特定K +通道阻滞剂以减少糖尿病患者体重增加和降低血糖的新概念。

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