Insulin‐stimulated chemokinesis in normal human neutrophils is dependent on D‐glucose concentration and sensitive to inhibitors of tyrosine kinase and phosphatidylinositol 3‐kinase

Insulin‐stimulated chemokinesis in normal human neutrophils is dependent on D‐glucose concentration and sensitive to inhibitors of tyrosine kinase and phosphatidylinositol 3‐kinase
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DOI:
10.1002/jlb.63.2.203
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发表时间:
1998-02
影响因子:
5.5
通讯作者:
P. Oldenborg;J. Sehlin
P. Oldenborg;J. Sehlin
中科院分区:
医学3区
文献类型:
--
作者:
P. Oldenborg;J. Sehlin

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这项研究表明,D-葡萄糖和胰岛素单独或某些组合对健康人的中性粒细胞具有化学动力学作用。胰岛素的刺激化学动力学作用在 40-160 μU/mL 胰岛素下存在,但仅在 5 mM D-葡萄糖存在下存在,而在 15 mM D-葡萄糖存在下则不存在。单独的 D-葡萄糖剂量依赖性地增加中性粒细胞运动,在 5-15 mM 时显示出最大效果,并在 25 mM 葡萄糖时恢复到基础运动。由于单独使用 5 和 15 mM D-葡萄糖的刺激化学动力学作用是相同的,因此高葡萄糖水平似乎不会抑制细胞的基本运动特性,但可能会产生细胞内信号,干扰胰岛素作用下的信号转导。酪氨酸激酶抑制剂金雀异黄酮或磷脂酰肌醇 3 激酶抑制剂渥曼青霉素在 5 mM D-葡萄糖存在下消除了 160 μU/mL 胰岛素的趋化动力学作用。这表明胰岛素对运动的影响确实是由受体相关酪氨酸激酶激活介导的,并涉及磷脂酰肌醇 3-激酶。 J.洛科克。生物。 63:203-208; 1998.
This study shows that D‐glucose and insulin, alone and in certain combinations, have chemokinetic effects on neutrophil granulocytes from healthy humans. A stimulatory chemokinetic effect of insulin was present at 40‐160 μU/mL insulin but only in the presence of 5 mM, and not at 15 mM, D‐glucose. D‐Glucose alone dose‐dependently increased the neutrophil locomotion, showing a maximum effect at 5–15 mM and a return toward the basal locomotion at 25 mM glucose. Because the stimulatory chemokinetic effects of 5 and 15 mM D‐glucose alone were the same, it seems that the high glucose level does not inhibit the basic motile properties of the cells but may generate intracellular signals interfering with the signal transduction underlying the insulin effect. The tyrosine kinase inhibitor, genistein, or the phosphatidylinositol 3‐kinase inhibitor, wortmannin, abolished the chemokinetic effect of 160 μU/mL insulin in the presence of 5 mM D‐glucose. This indicates that the insulin effect on locomotion is indeed mediated by receptor‐associated tyrosine kinase activation and involving phosphatidylinositol 3‐kinase. J. Leukoc. Biol. 63: 203–208; 1998.