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Reconstitution of Gluxotoxic HIT-T15 Cells With Somatostatin Transcription Factor-1 Partially Restores Insulin Promoter Activity

机译:生长抑素转录因子-1的光毒性HIT-T15细胞的重建部分恢复了胰岛素的启动子活性。

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摘要

We have reported that chronic culture of HIT-T15 cells inmedium containing supraphysiologic glucose con- centrations (11.1 mmol/l) causes a decrease in insulin mRNA levels, insulin content, and insulin release. Fur- thermore, decrease in insulin gene transcription and binding activity of two essential β-cell transcription factor, somatostatin transcription factor-1 (SFT-1; also known as GSTF, IDX-1, IPF-1, PDX-1, and GSF) and RIPE-3b1 activator, are associated with this glucotoxic Effect.
机译:我们已经报道,含有超生理学葡萄糖浓度(11.1 mmol / l)的HIT-T15细胞培养基的长期培养会导致胰岛素mRNA水平,胰岛素含量和胰岛素释放减少。此外,胰岛素基因转录的降低和两种必需的β细胞转录因子,生长抑素转录因子-1(SFT-1;也称为GSTF,IDX-1,IPF-1,PDX-1和GSF的结合活性) )和RIPE-3b1激活剂与这种糖毒作用有关。

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