Tsukahara F, Uchida Y, Ohba K, Ogawa A, Yoshioka T, Muraki T
Department of Pharmacology, Tokyo Women's Medical University, School of Medicine, Japan.
Jpn J Pharmacol. 1998 Jul;77(3):247-9. doi: 10.1254/jjp.77.247.
Abnormal regulation of mitochondrial uncoupling protein (UCP) gene expression was studied in brown adipose tissue (BAT) of monosodium glutamate (MSG)-induced obese mice. UCP mRNA levels in control mice increased markedly after acute cold exposure; however, MSG-obese mice showed an impaired response. In contrast, an injection of norepinephrine (NE) induced a comparable increase in UCP mRNA levels in control and MSG-obese mice. These results suggest that the impairment in the cold-induced increase in UCP mRNA is due to a deficient sympathetic input to BAT and/or to a diminished response of BAT to endogenous NE, which constitutes the mechanism of impaired thermoregulation in obese mice in a cold environment.
在味精(MSG)诱导的肥胖小鼠的棕色脂肪组织(BAT)中,研究了线粒体解偶联蛋白(UCP)基因表达的异常调控。急性冷暴露后,对照小鼠的UCP mRNA水平显著升高;然而,MSG诱导的肥胖小鼠表现出反应受损。相反,注射去甲肾上腺素(NE)可使对照小鼠和MSG诱导的肥胖小鼠的UCP mRNA水平产生类似的升高。这些结果表明,冷诱导的UCP mRNA升高受损是由于BAT的交感神经输入不足和/或BAT对内源性NE的反应减弱,这构成了肥胖小鼠在寒冷环境中体温调节受损的机制。