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首页> 外文期刊>American Journal of Physiology >Insulin and IGF-I inhibit calcium-dependent chloride secretion by T84 human colonic epithelial cells.
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Insulin and IGF-I inhibit calcium-dependent chloride secretion by T84 human colonic epithelial cells.

机译：胰岛素和IGF-1抑制T84人结肠上皮细胞分泌的钙依赖性氯离子。

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摘要

D-Myo-inositol (3,4,5,6) tetrakisphosphate [Ins(3,4,5,6)P(4)] or phosphatidylinositol 3-kinase (PI 3-kinase) activity acts to inhibit calcium-dependent chloride secretion in T84 colonic epithelial cells. To further distinguish between the contributions of these two signaling pathways to the inhibition of secretion, we studied effects of insulin, because the insulin receptor links to PI 3-kinase but not to pathways postulated to generate Ins(3,4,5,6)P(4). Chloride secretion across T84 cell monolayers was studied in Ussing chambers. Activation of PI 3-kinase was assessed by Western blotting. Basolateral, but not apical, addition of insulin inhibited carbachol- and thapsigargin-induced chloride secretion in a time- and concentration-dependent fashion. Insulin-like growth factor-I (IGF-I) had similar effects. Insulin had no effect on Ins(3,4,5,6)P(4) levels, and the inhibitory effects of insulin and IGF-I on chloride secretion were fully reversed by the PI 3-kinase inhibitors wortmannin and LY-294002. Western blot analysis showed that both insulin and IGF-I recruited the 85-kDa regulatory and 110-kDa catalytic subunits of PI 3-kinase to anti-phosphotyrosine immunoprecipitates. In conclusion, insulin and IGF-I act to inhibit calcium-dependent chloride secretion through a PI 3-kinase-dependent pathway. Because insulin is released in a pulsatile fashion postprandially and IGF-I levels are elevated in pathological settings, our findings may have physiological and/or pathophysiological significance.
机译：D-肌醇（3,4,5,6）四磷酸[Ins（3,4,5,6）P（4）]或磷脂酰肌醇3-激酶（PI 3-激酶）活性可抑制钙依赖性氯化物T84结肠上皮细胞中的分泌。为了进一步区分这两个信号通路对分泌抑制的贡献，我们研究了胰岛素的作用，因为胰岛素受体与PI 3-激酶连锁，但与假定产生Ins（3,4,5,6）的通路无关。 P（4）。在Ussing室研究了跨T84细胞单层的氯化物分泌。通过蛋白质印迹评估PI 3-激酶的活化。基底外侧但不是顶端的胰岛素的添加以时间和浓度依赖性方式抑制了卡巴胆碱和毒胡萝卜素诱导的氯化物分泌。胰岛素样生长因子-I（IGF-I）具有相似的作用。胰岛素对Ins（3,4,5,6）P（4）的水平没有影响，并且PI 3-激酶抑制剂渥曼青霉素和LY-294002完全逆转了胰岛素和IGF-I对氯化物分泌的抑制作用。 Western印迹分析表明，胰岛素和IGF-I均募集了PI 3激酶的85-kDa调节亚基和110-kDa催化亚基来抗磷酸酪氨酸免疫沉淀。总之，胰岛素和IGF-I通过PI 3激酶依赖性途径来抑制钙依赖性氯的分泌。由于胰岛素在餐后以脉动的方式释放并且在病理情况下IGF-I水平升高，因此我们的发现可能具有生理和/或病理生理意义。

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