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首页> 外文期刊>American Journal of Physiology >KATP channel-deficient pancreatic beta-cells are streptozotocin resistant because of lower GLUT2 activity
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KATP channel-deficient pancreatic beta-cells are streptozotocin resistant because of lower GLUT2 activity

机译：由于较低的GLUT2活性，KATP通道缺陷的胰腺β细胞具有链脲佐菌素抗性

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First published November 27, 2007; doi:10.1152/ajpendo.00296.2007.-In wild-type mice, a single injection of streptozotocin (STZ, 200 mg/kg body wt) caused within 4 days severe hyperglycemia, hypoinsuline-mia, significant glucose intolerance, loss of body weight, and the disappearance of pancreatic beta-cells. However, in ATP-sensitive K+ channel (Katp channefj-deficient mice (Kir6.2~(-/-) mice), STZ had none of these effects. Exposing isolated pancreatic islets to STZ caused severe damage in wild-type but not in Kir6.2~(-/-) islets. Following a single injection, plasma STZ levels were slightly less in Kir6.2~(-/-) mice than in wild-type mice. Despite the difference in plasma STZ, wild-type and Kir6.2~(-/-) liver accumulated the same amount of STZ, whereas Kir6.2~(-/-) pancreas accumulated 4.1-fold less STZ than wild-type pancreas. Kir6.2~(-/-) isolated pancreatic islets also transported less glucose than wild-type ones. Quantification of glucose transporter 2 (GLUT2) protein content by Western blot using an antibody with an epitope in the extracellular loop showed no significant difference in GLUT2 content between wild-type and Kir6.2~(-/-) pancreatic islets. However, visualization by immunofluorescence with the same antibody gave rise to 32% less fluorescence in Kir6.2~(-/-) pancreatic islets. The fluorescence intensity using another antibody, with an epitope in the COOH terminus, was 5.6 times less in Kir66.2~(-/-) than in wild-type pancreatic islets. We conclude that 1) Kir~(-/-) mice are STZ resistant because of a decrease in STZ transport by GLUT2 in pancreatic beta-cells and 2) the decreased transport is due to a downregulation of GLUT2 activity involving an effect at the COOH terminus.
机译：首次发布于2007年11月27日; doi：10.1152 / ajpendo.00296.2007.-在野生型小鼠中，单次注射链脲佐菌素（STZ，200 mg / kg体重）在4天内引起严重的高血糖，低胰岛素血症，严重的葡萄糖耐受不良，体重减轻，和胰腺β细胞的消失然而，在ATP敏感的K +通道（Katp channefj缺陷小鼠（Kir6.2〜（-/-）小鼠）中），STZ并没有这些作用。将分离的胰岛暴露于STZ会对野生型小鼠造成严重损害，但对野生型小鼠却没有造成严重损害。 Kir6.2〜（-/-）胰岛，单次注射后，Kir6.2〜（-/-）小鼠的血浆STZ水平比野生型小鼠略低，尽管血浆STZ，野生型和Kir6.2〜（-/-）肝脏的STZ含量相同，而Kir6.2〜（-/-）胰腺的STZ含量比野生型胰腺少4.1倍。分离的胰岛也转运的葡萄糖少于野生型的胰岛，通过蛋白质印迹法对葡萄糖转运蛋白2（GLUT2）的蛋白质含量进行了定量，结果显示在野生型和Kir6之间，GLUT2的含量没有明显差异。 2〜（-/-）胰岛，但是，用相同的抗体通过免疫荧光观察后，Kir6.2〜（-/-）胰岛的荧光减少了32％ ets。使用另一种在COOH末端具有表位的抗体，其荧光强度在Kir66.2〜（-/-）中比野生型胰岛小5.6倍。我们得出的结论是：1）Kir〜（-/-）小鼠对STZ耐药，原因是胰腺β细胞中GLUT2的STZ转运减少，并且2）转运减少是由于GLUT2活性下调所致，涉及COOH的作用总站。

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