Differential sensitivity of GLUT1-and GLUT2-expressing β cells to streptozotocin
Differential sensitivity of GLUT1-and GLUT2-expressing β cells to streptozotocin
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DOI：
10.1006/bbrc.2001.6145
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发表时间：
2001-12-21
影响因子：
3.1
通讯作者：
Thorens, B
中科院分区：
文献类型：
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作者：
Hosokawa, M;Dolci, W;Thorens, B
动物注射链脲佐菌素会破坏胰岛β细胞，导致胰岛素缺乏性糖尿病。在这里，我们评估了链脲佐菌素(STZ)对在大鼠胰岛素启动子(分别为RIPG1 x G2(-/-)和RIPG2 X G2(-/-)小鼠)下重新表达GLUT1或GLUT2的GLUT2(-/-)小鼠的毒性作用。我们证明，在RIFPG2X G2(-/-)小鼠体内注射STZ会引起高血糖(>；20 mM)，并使胰腺胰岛素含量减少80%。在体外，RIFPG2 X G2(-/-)胰岛的存活率也显著降低。相比之下，STZ没有引起RIPG1 X G2(-/-)小鼠的高血糖，也没有降低胰腺胰岛素含量。体外培养的RIPG1XG2(-/-)胰岛活力也不受STZ的影响。由于每种类型转基因小鼠的胰岛在功能上无法区分，这些数据有力地支持了STZ对0细胞的毒性取决于GLUT2表达的观点。(C)2001年爱思唯尔科学公司。
Streptozotocin injection in animals destroys pancreatic beta cells, leading to insulinopenic diabetes. Here, we evaluated the toxic effect of streptozotocin (STZ) in GLUT2(-/-) mice reexpressing either GLUT1 or GLUT2 in their 13 cells under the rat insulin promoter (RIPG1 x G2(-/-) and RIPG2 X G2(-/-) mice, respectively). We demonstrated that injection of STZ into RIFPG2 X G2(-/-) mice induced hyperglycemia (>20 mM) and an similar to80% reduction in pancreatic insulin content. In vitro, the viability of RIFPG2 X G2(-/-) islets was also strongly reduced. In contrast, STZ did not induce hyperglycemia in RIPG1 X G2(-/-) mice and did not reduce pancreatic insulin content. The viability of in vitro cultured RIPG1 X G2(-/-) islets was also unaffected by STZ. As islets from each type of transgenic mice were functionally indistinguishable, these data strongly support the notion that STZ toxicity toward 0 cells depends on the expression of GLUT2. (C) 2001 Elsevier Science.