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首页> 外文期刊>Life sciences >OVEREXPRESSION OF BOVINE GROWTH HORMONE IN TRANSGENIC MICE IS ASSOCIATED WITH CHANGES IN HEPATIC INSULIN RECEPTORS AND IN THEIR KINASE ACTIVITY
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OVEREXPRESSION OF BOVINE GROWTH HORMONE IN TRANSGENIC MICE IS ASSOCIATED WITH CHANGES IN HEPATIC INSULIN RECEPTORS AND IN THEIR KINASE ACTIVITY

机译：牛生长激素在转基因小鼠中的过表达与肝胰岛素受体的变化及其激酶活性有关

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Transgenic mice expressing a hybrid gene produced by linking the promoter regulatory region of phosphoenolpyruvate carboxykinase (PEPCK) gene to the bovine growth hormone (bGH) gene, were used to investigate the effects of GH on insulin binding and insulin dependent tyrosine kinase activity of hepatic insulin receptors. Transgenic mice had normal levels of blood glucose, despite hyperinsulinemia, indicating that these animals were insulin resistant. The number of insulin receptors in the liver of transgenic mice was significantly decreased in both the particulate fraction (25%) and the solubilized membranes (40%) indicating that expressed (functional) and non-expressed (cryptic) receptors were affected. Scatchard analysis of competitive binding curves for insulin indicated that the affinity of the receptor did not differ between transgenic and normal mice. Insulin dependent tyrosine kinase activity in insulin receptors partially purified by wheat germ agglutin (WGA) agarose chromatography from solubilized liver membranes, was measured. The stimulatory action of insulin on phosphorylation of the synthetic substrate (a copolymer Glu-Tyr, 4:1) was increased 100% in transgenic, as compared to normal mice, using the same binding activity. Since transgenic mice are hyperinsulinemic, it is likely that the decreased insulin binding in this group reflects down regulation of the expressed and non-expressed insulin receptors, and the increased kinase activity represents a compensatory mechanism. We conclude that alterations in the insulin receptor number and in the tyrosine kinase activity develop in response to changes in insulin levels. Thus, insulin resistance detected in the liver of transgenic mice overexpressing GH may be due to post receptor defects. [References: 30]
机译：使用表达通过将磷酸烯醇丙酮酸羧激酶（PEPCK）的启动子调控区与牛生长激素（bGH）基因连接而产生的杂种基因的转基因小鼠，研究GH对肝胰岛素的胰岛素结合和胰岛素依赖性酪氨酸激酶活性的影响受体。尽管有高胰岛素血症，转基因小鼠的血糖水平却正常，表明这些动物具有胰岛素抵抗性。转基因小鼠肝脏中胰岛素受体的数量在颗粒部分（25％）和溶解膜（40％）中均显着减少，表明表达（功能）和未表达（隐性）受体均受到影响。胰岛素竞争性结合曲线的Scatchard分析表明，转基因小鼠和正常小鼠之间受体的亲和力没有差异。测量了通过小麦胚芽凝集素（WGA）琼脂糖色谱法从溶解的肝膜中部分纯化的胰岛素受体中的胰岛素依赖性酪氨酸激酶活性。与正常小鼠相比，使用相同的结合活性，与正常小鼠相比，胰岛素对合成底物（共聚物Glu-Tyr，4：1）磷酸化的刺激作用提高了100％。由于转基因小鼠是高胰岛素血症的，因此这一组中胰岛素结合的减少很可能反映了表达和未表达的胰岛素受体的下调，并且激酶活性的增加代表了一种补偿机制。我们得出结论，胰岛素受体数量和酪氨酸激酶活性的变化是根据胰岛素水平的变化而发展的。因此，在过表达GH的转基因小鼠的肝脏中检测到的胰岛素抗性可能是由于受体后缺陷引起的。 [参考：30]

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