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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The role of PI 3-kinase in EGF-stimulated jejunal glucose transport.
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The role of PI 3-kinase in EGF-stimulated jejunal glucose transport.

机译：PI 3-激酶在EGF刺激的空肠葡萄糖转运中的作用。

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摘要

Epidermal growth factor (EGF) rapidly increases jejunal glucose transport. Signal transduction mechanisms mediating EGF-induced alterations in jejunal glucose transport remain to be determined. New Zealand White rabbit (1 kg) jejunal tissue was stripped and mounted in short-circuited Ussing chambers. The transport of tritiated 3-O-methylglucose was measured in the presence of the PKC agonist 1,2-dioctanoyl-sn-glycerol (1,2-DOG) or the inactive analog 1,3-dioctanoyl-sn-glycerol (1,3-DOG). Additional experiments examined the effect of the PKC inhibitor chelerythrine, the PLC inhibitor U73122, the MAPK inhibitor PD 98059, the G-protein inhibitor GDP-betaS, the PI 3-kinase inhibitor LY294002, or the microtubule inhibitor colchicine on EGF-induced jejunal glucose transport. Net jejunal 3-O-methylglucose absorption was significantly increased following specific activation of PKC. A PKC antagonist inhibited the EGF-induced increase in net 3-O-methylglucose transport, while PI 3-kinase inhibition completely blocked the EGF-induced transport increase. Inhibition of PLC, MAPK, G-proteins, and microtubules had no effect on EGF-stimulated increases in jejunal transport. We conclude that the effect of EGF on jejunal glucose transport is mediated at least in part by PKC and PI 3-kinase.
机译：表皮生长因子（EGF）迅速增加空肠葡萄糖转运。介导EGF诱导的空肠葡萄糖转运改变的信号转导机制尚待确定。剥去新西兰白兔（1kg）的空肠组织，并将其安装在短路的Ussing室中。在PKC激动剂1,2-二辛酰基-sn-甘油（1,2-DOG）或非活性类似物1,3-二辛酰基-sn-甘油（1， 3-DOG）。其他实验检查了PKC抑制剂白屈菜红碱，PLC抑制剂U73122，MAPK抑制剂PD 98059，G蛋白抑制剂GDP-betaS，PI 3-激酶抑制剂LY294002或微管抑制剂秋水仙碱对EGF诱导的空肠葡萄糖的影响运输。在PKC特异性激活后，空肠3-O-甲基葡萄糖的净吸收显着增加。 PKC拮抗剂抑制EGF诱导的3-O-甲基葡萄糖净转运增加，而PI 3-激酶抑制则完全阻止EGF诱导的转运增加。抑制PLC，MAPK，G蛋白和微管对EGF刺激的空肠转运增加没有影响。我们得出结论，EGF对空肠葡萄糖转运的作用至少部分由PKC和PI 3-激酶介导。

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