Hidaka S, Yoshimatsu H, Kakuma T, Sakino H, Kondou S, Hanada R, Oka K, Teshima Y, Kurokawa M, Sakata T
Department of Internal Medicine I, School of Medicine, Oita Medical University, Oita, 879-5593, Japan.
Proc Soc Exp Biol Med. 2000 Jul;224(3):172-7. doi: 10.1046/j.1525-1373.2000.22417.x.
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.
链脲佐菌素(STZ)诱导的糖尿病大鼠对冷应激的易感性已经得到证实。控制体温的要素之一是产热,其中解偶联蛋白(UCP)已知发挥重要作用。我们研究了大鼠STZ诱导糖尿病的急性和慢性阶段棕色脂肪组织(BAT)、白色脂肪组织(WAT)和骨骼肌(MSL)中UCP2和UCP3的表达。长期影响以及此后胰岛素治疗的影响此前也未被探索,本研究对此进行了考察。在糖尿病急性期(STZ注射后2.5天),BAT、WAT和MSL中UCP2基因表达以及肌肉中UCP3表达显著增加。在糖尿病慢性期(STZ注射后21天),无胰岛素补充时MSL中UCP2和UCP3表达恢复到对照水平。慢性期BAT和WAT中的UCP2保持高水平,而BAT和WAT中UCP3表达在急性期未改变,却显著降低。胰岛素补充使BAT和WAT中UCP2表达恢复,但使WAT中UCP3表达过度校正至对照水平以上,且不影响BAT中UCP3表达。胰岛素补充使MSL中UCP3表达低于对照水平。这些结果表明,STZ诱导的糖尿病对UCPs基因表达的影响具有组织特异性且取决于糖尿病持续时间。