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糖尿病GK大鼠血浆而非正常Wistar大鼠血浆可诱导GK大鼠主动脉原代培养平滑肌细胞中胰岛素刺激的DNA合成。

Diabetic GK rat plasma but not normal Wistar rat plasma induces insulin-stimulated DNA synthesis in primary cultured smooth muscle cells in GK rat aorta.

作者信息

Kimura I, Nakano Y, Naitoh T, Okabe M, Kimura M

机构信息

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.

出版信息

Jpn J Pharmacol. 1994 Mar;64(3):195-200. doi: 10.1254/jjp.64.195.

DOI:10.1254/jjp.64.195
PMID:8022121
Abstract

We investigated the effect of diabetic plasma on insulin-stimulated DNA synthesis in primary cultured aortic smooth muscle cells (SMC) of the GK rat, a model of non-insulin-dependent diabetes mellitus, and compared it with that of Wistar normal rat plasma. We measured the incorporation of 3H-thymidine into cultured SMC. The diabetic plasma (3%) of GK rat, but neither the plasma (3%) of Wistar normal rat nor the plasma (3%) (not containing both insulin-like growth factor-I (IGF-I) and corticosterone) of Wistar hypophysectomized rat induced insulin-stimulated DNA synthesis in GK rat SMC. The responsiveness of SMC to insulin, not to IGF-I, was decreased remarkably by the diabetic state. The diabetic plasma of GK rat remarkably enhanced and the plasma of Wistar hypophysectomized rat weakly enhanced insulin-stimulated DNA synthesis in Wistar normal rat SMC. Corticosterone (20 nM) increased insulin-stimulated DNA synthesis in GK rat SMC but decreased it in Wistar normal rat SMC, using the plasma of Wistar hypophysectomized rat. Corticosterone levels were lower in GK rat plasma than in normal Wistar rat plasma. These results demonstrate that the enhancement of insulin-stimulated DNA synthesis in diabetic SMC by the diabetic plasma of GK rat may be due to neither IGF-I nor corticosterone but due to other factors.

摘要

我们研究了糖尿病血浆对GK大鼠(一种非胰岛素依赖型糖尿病模型)原代培养的主动脉平滑肌细胞(SMC)中胰岛素刺激的DNA合成的影响,并将其与Wistar正常大鼠血浆的影响进行了比较。我们测量了3H-胸腺嘧啶核苷掺入培养的SMC中的情况。GK大鼠的糖尿病血浆(3%)可诱导GK大鼠SMC中胰岛素刺激的DNA合成,而Wistar正常大鼠的血浆(3%)或Wistar去垂体大鼠的血浆(3%)(不含胰岛素样生长因子-I(IGF-I)和皮质酮)均不能诱导。糖尿病状态显著降低了SMC对胰岛素而非IGF-I的反应性。GK大鼠的糖尿病血浆显著增强了Wistar正常大鼠SMC中胰岛素刺激的DNA合成,而Wistar去垂体大鼠的血浆则微弱增强了该反应。使用Wistar去垂体大鼠的血浆时,皮质酮(20 nM)增加了GK大鼠SMC中胰岛素刺激的DNA合成,但降低了Wistar正常大鼠SMC中胰岛素刺激的DNA合成。GK大鼠血浆中的皮质酮水平低于正常Wistar大鼠血浆中的水平。这些结果表明,GK大鼠的糖尿病血浆增强糖尿病SMC中胰岛素刺激的DNA合成可能既不是由于IGF-I也不是由于皮质酮,而是由于其他因素。

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