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首页> 外文期刊>American Journal of Physiology >Involvement of PI 3-kinase in IGF-I stimulation of jejunal Na+-K+-ATPase activity and nutrient absorption.
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Involvement of PI 3-kinase in IGF-I stimulation of jejunal Na+-K+-ATPase activity and nutrient absorption.

机译：PI 3-激酶参与IGF-I刺激空肠Na + -K + -ATPase活性和养分吸收。

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摘要

Mechanisms responsible for increased jejunal transport rates observed in tissues treated with orally administered insulin-like growth factor-I (IGF-I) were studied in 5-day-old colostrum-deprived piglets. Human recombinant IGF-I (3.5 mg. kg(-1). day(-1)) or control vehicle was given orogastrically for 4 days. Disaccharidase activity, fructose uptake, and Na+-glucose cotransporter SGLT-1 protein abundance were similar between groups. Oral IGF-I produced greater rates of enterocyte Na+-K+-ATPase activity with no significant differences in Na+-K+-ATPase abundance. Cellular mechanisms responsible for transport changes were studied in Ussing chambers. In control tissues, the presence of IGF-I in mucosal solutions increased basal short-circuit current (I(sc)), potential difference, D-glucose-stimulated I(sc), and Na+-K+-ATPase activity; these changes were abolished by preincubation of tissues with wortmannin, a phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor. The results suggest that the effect of IGF-I on jejunal ion and nutrient transport involves activation of PI 3-kinase and stimulation of Na+-K+-ATPase activity in enterocytes.
机译：在5天大的初乳剥夺型仔猪中研究了在口服胰岛素样生长因子-I（IGF-I）处理的组织中观察到的导致空肠运输速率增加的机制。经口胃给予人重组IGF-I（3.5 mg。kg（-1）。day（-1））或对照载体4天。两组之间的糖精酶活性，果糖摄取和Na +-葡萄糖共转运蛋白SGLT-1蛋白的丰度相似。口服IGF-I产生的肠细胞Na + -K + -ATPase活性更高，而Na + -K + -ATPase的丰度没有显着差异。在Ussing室内研究了负责运输变化的细胞机制。在对照组织中，粘膜溶液中IGF-I的存在增加了基础短路电流（I（sc）），电势差，D-葡萄糖刺激的I（sc）和Na + -K + -ATPase活性。通过用渥曼青霉素（一种磷脂酰肌醇3-激酶（PI 3-激酶）抑制剂）对组织进行预孵育，可以消除这些变化。结果表明，IGF-I对空肠离子和营养物转运的作用涉及激活PI 3-激酶和刺激肠上皮细胞Na + -K + -ATPase活性。

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