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首页> 外文期刊>Molecular and Cellular Biology >Glucose transporter isotypes switch in T-antigen-transformed pancreatic beta cells growing in culture and in mice.
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Glucose transporter isotypes switch in T-antigen-transformed pancreatic beta cells growing in culture and in mice.

机译：葡萄糖转运蛋白同种型在培养和小鼠中生长的经T抗原转化的胰岛β细胞中转换。

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High-level expression of the low-Km glucose transporter isoform GLUT-1 is characteristic of many cultured tumor and oncogene-transformed cells. In this study, we tested whether induction of GLUT-1 occurs in tumors in vivo. Normal mouse beta islet cells express the high-Km (approximately 20 mM) glucose transporter isoform GLUT-2 but not the low-Km (1 to 3 mM) GLUT-1. In contrast, a beta cell line derived from an insulinoma arising in a transgenic mouse harboring an insulin-promoted simian virus 40 T-antigen oncogene (beta TC3) expressed very low levels of GLUT-2 but high levels of GLUT-1. GLUT-1 protein was not detectable on the plasma membrane of islets or tumors of the transgenic mice but was induced in high amounts when the tumor-derived beta TC3 cells were grown in tissue culture. GLUT-1 expression in secondary tumors formed after injection of beta TC3 cells into mice was reduced. Thus, high-level expression of GLUT-1 in these tumor cells is characteristic of culture conditions and is not induced by the oncogenic transformation; indeed, overnight culture of normal pancreatic islets causes induction of GLUT-1. We also investigated the relationship between expression of the different glucose transporter isoforms by islet and tumor cells and induction of insulin secretion by glucose. Prehyperplastic transgenic islet cells that expressed normal levels of GLUT-2 and no detectable GLUT-1 exhibited an increased sensitivity to glucose, as evidenced by maximal insulin secretion at lower glucose concentrations, compared with that exhibited by normal islets. Further, hyperplastic islets and primary and secondary tumors expressed low levels of GLUT-2 and no detectable GLUT-1 on the plasma membrane; these cells exhibited high basal insulin secretion and responded poorly to an increase in extracellular glucose. Thus, abnormal glucose-induced secretion of insulin in prehyperplastic islets in mice was independent of changes in GLUT-2 expression and did not require induction of GLUT-1 expression.
机译：低Km葡萄糖转运蛋白同工型GLUT-1的高水平表达是许多培养的肿瘤和癌基因转化细胞的特征。在这项研究中，我们测试了GLUT-1的诱导是否在体内肿瘤中发生。正常小鼠β胰岛细胞表达高Km（约20 mM）葡萄糖转运蛋白同工型GLUT-2，但不表达低Km（1至3 mM）GLUT-1。相反，源自具有胰岛素促进的猿猴病毒40 T-抗原致癌基因（βTC3）的转基因小鼠中产生的胰岛素瘤的β细胞系表达极低水平的GLUT-2，但表达高水平的GLUT-1。 GLUT-1蛋白在转基因小鼠的胰岛或肿瘤的质膜上无法检测到，但是当在组织培养物中生长肿瘤衍生的βTC3细胞时，其被大量诱导。 βTC3细胞注入小鼠后形成的继发性肿瘤中GLUT-1表达降低。因此，在这些肿瘤细胞中GLUT-1的高水平表达是培养条件的特征，而不是由致癌性转化诱导的。实际上，正常胰岛的过夜培养会引起GLUT-1的诱导。我们还研究了胰岛和肿瘤细胞表达不同的葡萄糖转运蛋白同工型与葡萄糖诱导胰岛素分泌之间的关系。与正常胰岛相比，表达正常水平的GLUT-2而没有可检测到的GLUT-1的增生前转基因胰岛细胞对葡萄糖的敏感性增加，这是在较低葡萄糖浓度下最大胰岛素分泌所证明的。此外，增生的胰岛以及原发性和继发性肿瘤在细胞膜上表达的GLUT-2水平低，而未检测到GLUT-1。这些细胞表现出较高的基础胰岛素分泌，并且对细胞外葡萄糖的增加反应较差。因此，异常葡萄糖诱导的小鼠增生前胰岛中胰岛素的分泌独立于GLUT-2表达的变化，并且不需要诱导GLUT-1表达。

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