Tiedge M, Höhne M, Lenzen S
Institute of Pharmacology and Toxicology, University of Göttingen, Germany.
Biochem J. 1993 Nov 15;296 ( Pt 1)(Pt 1):113-8. doi: 10.1042/bj2960113.
The insulin-secretory response to glucose is defective in the RINm5F insulin-producing tumour cell line. Stable transfection with human low-affinity GLUT2 glucose-transporter cDNA revealed a significant improvement in stimulus-secretion coupling in these insulinoma cells. 3-O-Methylglucose uptake increased 10-fold in the concentration range 10-20 mM, whereas non-transfected control cells were unresponsive. Northern-blot analysis revealed a 7-fold increase in expression of the insulin gene in the GLUT2-transfected RINm5F cell clone T1. In contrast, glucokinase and GLUT1 glucose-transporter mRNA gene expression were not affected by transfection with GLUT2 glucose-transporter cDNA. The insulin content of transfected RINm5F cells was 7-fold higher after tissue culture at high glucose concentrations than in non-transfected controls. GLUT2-transfected RINm5F cells also regained insulin-secretory responsiveness toward high glucose concentrations. Tissue culture for 72 h in 20 mM glucose induced glucokinase activity in the GLUT2-transfected RINm5F clone T1, raising the glucokinase/hexokinase phosphorylation ratio from 0.2 to 0.6. The experiments demonstrate that an increased glucose uptake via a low-affinity glucose transporter and an increased metabolic flux rate are important factors in the induction of insulin-gene expression and glucokinase activity and thus improved glucose-induced biosynthesis and secretion of insulin in RINm5F insulinoma cells.
在RINm5F胰岛素产生肿瘤细胞系中,对葡萄糖的胰岛素分泌反应存在缺陷。用人类低亲和力GLUT2葡萄糖转运体cDNA进行稳定转染后,这些胰岛素瘤细胞的刺激-分泌偶联有显著改善。在10-20 mM浓度范围内,3-O-甲基葡萄糖摄取增加了10倍,而未转染的对照细胞无反应。Northern印迹分析显示,在GLUT2转染的RINm5F细胞克隆T1中,胰岛素基因的表达增加了7倍。相比之下,葡萄糖激酶和GLUT1葡萄糖转运体mRNA基因表达不受GLUT2葡萄糖转运体cDNA转染的影响。在高葡萄糖浓度下进行组织培养后,转染的RINm5F细胞的胰岛素含量比未转染的对照高7倍。GLUT2转染的RINm5F细胞也恢复了对高葡萄糖浓度的胰岛素分泌反应性。在20 mM葡萄糖中进行72小时的组织培养可诱导GLUT2转染的RINm5F克隆T1中的葡萄糖激酶活性,使葡萄糖激酶/己糖激酶磷酸化比率从0.2提高到0.6。这些实验表明,通过低亲和力葡萄糖转运体增加葡萄糖摄取以及增加代谢通量率是诱导胰岛素基因表达和葡萄糖激酶活性的重要因素,从而改善了RINm5F胰岛素瘤细胞中葡萄糖诱导的胰岛素生物合成和分泌。