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PI3 kinase and PDK1 in the regulation of the electrogenic intestinal dipeptide transport

机译：PI3激酶和PDK1在调节肠源性肠二肽运输中的作用

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摘要

The phosphoinositol 3 kinase (PI3K) and the phosphoinositide dependent kinase (PDK1) stimulate the serum and glucocorticoid inducible kinase (SGK) and protein kinase B (PKB/Akt) isoforms, kinases stimulating a variety of transporters. Most recently, SGK1 was shown to stimulate the peptide transporters PepT1 and PepT2, and to mediate the glucocorticoid stimulation of PepT1. Basal electrogenic intestinal peptide transport was, however, not dependent on the presence of SGK1. The present study explored whether basal electrogenic intestinal peptide transport is dependent on PI3K or PDK1. To this end, peptide transport in intestinal segments was determined utilizing Ussing chamber analysis. Cytosolic pH (pH_i) was determined by BCECF fluorescence. The luminal addition of 5 mM dipeptide gly-gly induced a current (Ip) across intestinal segments. Ip was significantly decreased in the presence of PI3 kinase inhibitors Wortmannin (1 μM) or LY294002 (50 μM). Exposure of isolated intestinal cells to 5 mM gly-gly was followed by cytosolic acidification (ΔpH_i), which was significantly blunted by Wortmannin and by LY294002. Both, Ip and ΔpHi were significantly smaller in PDK1 hypomorphic mice (pdk~(1flfl)) than in their wild type littermates (pdk1~(wt)). In conclusion, PI3K and PDK1 participate in the regulation of basal peptide transport.
机译：磷酸肌醇3激酶（PI3K）和磷酸肌醇依赖性激酶（PDK1）刺激血清和糖皮质激素诱导激酶（SGK）和蛋白激酶B（PKB / Akt）亚型，这些激酶刺激多种转运蛋白。最近，显示SGK1刺激肽转运蛋白PepT1和PepT2，并介导糖皮质激素对PepT1的刺激。然而，基础电肠肽运输不依赖于SGK1的存在。本研究探讨了基础电源性肠肽转运是否依赖于PI3K或PDK1。为此，利用Ussing chamber分析确定肠段中的肽运输。通过BCECF荧光测定胞质pH（pH_i）。腔内添加5 mM二肽gly-gly会在肠段产生电流（Ip）。在PI3激酶抑制剂Wortmannin（1μM）或LY294002（50μM）存在下，Ip明显降低。将分离的肠道细胞暴露于5 mM gly-gly，然后进行胞浆酸化（ΔpH_i），这被Wortmannin和LY294002明显削弱了。 Pdk1亚型小鼠（pdk〜（1flfl））的Ip和ΔpHi均明显低于其野生型同窝仔动物（pdk1〜（wt））。总之，PI3K和PDK1参与了基础肽转运的调节。

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