Regulation of human trophoblast GLUT1 glucose transporter by insulin-like growth factor I (IGF-I).
Regulation of human trophoblast GLUT1 glucose transporter by insulin-like growth factor I (IGF-I).
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DOI：
10.1371/journal.pone.0106037
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Illsley NP
中科院分区：
文献类型：
--
作者：
Baumann MU;Schneider H;Malek A;Palta V;Surbek DV;Sager R;Zamudio S;Illsley NP
葡萄糖通过胎盘通过屏障层、合体滋养层的微绒毛和基底膜的相对面上的葡萄糖转运蛋白向胎儿转运。虽然GLUT1葡萄糖转运体的基底膜含量似乎是胎盘转运的限速步骤，但调控转运体表达和活性的因素在很大程度上是未知的。鉴于许多研究表明IGF-I与胎儿生长有关，我们研究了IGF-I对胎盘葡萄糖转运和GLUT1转运体表达的影响。IGF-I诱导BeWo绒毛膜癌细胞GLUT1蛋白表达增加。基底外侧(但不是微绒毛)葡萄糖摄取增加，跨BeWo单层的葡萄糖跨上皮运输增加。经IGF-I处理的原代合体细胞也显示GLUT1蛋白表达增加。经IGF-I处理的足月胎盘组织合体基底膜GLUT1增加，而微绒毛膜GLUT1无明显变化。采用胎盘双灌流模型观察胎盘灌流IGF-I对胎盘葡萄糖转运和合体细胞GLUT1含量的影响。在对照灌注组，在灌流过程中胎盘葡萄糖转运减少，而在通过胎儿循环灌流IGF-I的组织中没有变化。来自IGF-I灌流组织的合胞基膜显示GLUT1含量增加。这些结果表明，无论是通过微绒毛受体还是通过基底膜受体，IGF-I都能增加基底膜GLUT1的含量，上调基底膜葡萄糖的转运，从而增加跨上皮糖的转运。这些观察为IGF-I在调节胎儿生长中控制营养供应的机制提供了部分解释。
Glucose transport to the fetus across the placenta takes place via glucose transporters in the opposing faces of the barrier layer, the microvillous and basal membranes of the syncytiotrophoblast. While basal membrane content of the GLUT1 glucose transporter appears to be the rate-limiting step in transplacental transport, the factors regulating transporter expression and activity are largely unknown. In view of the many studies showing an association between IGF-I and fetal growth, we investigated the effects of IGF-I on placental glucose transport and GLUT1 transporter expression. Treatment of BeWo choriocarcinoma cells with IGF-I increased cellular GLUT1 protein. There was increased basolateral (but not microvillous) uptake of glucose and increased transepithelial transport of glucose across the BeWo monolayer. Primary syncytial cells treated with IGF-I also demonstrated an increase in GLUT1 protein. Term placental explants treated with IGF-I showed an increase in syncytial basal membrane GLUT1 but microvillous membrane GLUT1 was not affected. The placental dual perfusion model was used to assess the effects of fetally perfused IGF-I on transplacental glucose transport and syncytial GLUT1 content. In control perfusions there was a decrease in transplacental glucose transport over the course of the perfusion, whereas in tissues perfused with IGF-I through the fetal circulation there was no change. Syncytial basal membranes from IGF-I perfused tissues showed an increase in GLUT1 content. These results demonstrate that IGF-I, whether acting via microvillous or basal membrane receptors, increases the basal membrane content of GLUT1 and up-regulates basal membrane transport of glucose, leading to increased transepithelial glucose transport. These observations provide a partial explanation for the mechanism by which IGF-I controls nutrient supply in the regulation of fetal growth.
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