Differential sensitivity of GLUT1-and GLUT2-expressing β cells to streptozotocin

被引：64

作者：

Hosokawa, M ^{[1
]}

Dolci, W ^{[1
]}

Thorens, B ^{[1
]}

机构：

[1] Univ Lausanne, Inst Pharmacol & Toxicol, CH-1005 Lausanne, Switzerland

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 289卷 / 05期

关键词：

insulin; streptozocin; pancreatic islets; GLUT1; GLUT2; diabetes;

D O I：

10.1006/bbrc.2001.6145

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：1114 / 1117

页数：4

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