Tissue-specific expression of the uncoupling protein family in streptozotocin-induced diabetic rats.

S. Hidaka, H. Yoshimatsu, T. Kakuma, H. Sakino, S. Kondou, R. Hanada, K. Oka, Y. Teshima, M. Kurokawa, T. Sakata
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引用次数: 24

Abstract

The vulnerability of streptozotocin (STZ)-induced diabetic rats to cold stress has been established. One of the elements controlling body temperature is thermogenesis, in which uncoupling protein (UCP) is known to play an important role. We have examined UCP2 and UCP3 expressions in brown adipose tissue (BAT), white adipose tissue (WAT), and skeletal muscle (MSL) during the acute and chronic phases of STZ-induced diabetes in rats. The long-term effect and the effect of insulin treatment thereafter were also unexplored previously and are examined in this study. In the acute phase of diabetes (2.5 days after STZ injection), UCP2 gene expression in BAT, WAT, and MSL, and UCP3 expression in the muscle were significantly increased. In the chronic phase of diabetes (21 days after STZ injection), UCP2 and UCP3 expression in the MSL were restored to the control levels without insulin supplementation. UCP2 in BAT and WAT remained high in the chronic phase, whereas UCP3 expression in BAT and WAT, which did not change in the acute phase, was significantly decreased. Insulin supplementation restored UCP2 expression in BAT and WAT, but over-corrected UCP3 in WAT above the control and did not affect UCP3 expression in BAT. Insulin supplementation depressed UCP3 expression in the MSL below control. These results indicate that the effects of STZ-induced diabetes on UCPs gene expression are tissue-specific as well as dependent on the duration of diabetes.
解偶联蛋白家族在链脲佐菌素诱导的糖尿病大鼠中的组织特异性表达。
链脲佐菌素(STZ)诱导的糖尿病大鼠对冷应激的易感性已被证实。控制体温的因素之一是产热作用,其中解偶联蛋白(UCP)被认为起着重要作用。我们检测了stz诱导的大鼠糖尿病急性期和慢性期棕色脂肪组织(BAT)、白色脂肪组织(WAT)和骨骼肌(MSL)中UCP2和UCP3的表达。长期效果和胰岛素治疗的效果也未被探索,并在本研究中进行了检查。在糖尿病急性期(注射STZ后2.5 d), BAT、WAT、MSL组织中UCP2基因表达和肌肉组织中UCP3表达均显著升高。在糖尿病慢慢性期(注射STZ后21 d),在不补充胰岛素的情况下,MSL中UCP2和UCP3的表达恢复到对照水平。BAT和WAT中UCP2在慢性期保持高表达,而BAT和WAT中UCP3的表达在急性期没有变化,但明显降低。补充胰岛素可恢复BAT和WAT中UCP2的表达,但过度纠正WAT中UCP3的表达高于对照组,不影响BAT中UCP3的表达。胰岛素补充抑制UCP3在对照组下的表达。这些结果表明,stz诱导的糖尿病对UCPs基因表达的影响是组织特异性的,并且依赖于糖尿病的持续时间。
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