Expression of UCP-2 and UCP-3 genes in obese type 2 diabetes mellitus and its modification by a cytokine inducer

UCP-2和UCP-3基因在肥胖2型糖尿病中的表达及细胞因子诱导剂对其的修饰KK-Ay小鼠是肥胖2型糖尿病的模型。CFA治疗显著改善了KK-Ay小鼠的葡萄糖耐受不良，并且这种改善通过IL-1来实现。与盐水处理的对照小鼠相比，CFA处理的KK-Ay小鼠体重减轻，即使食物摄入量没有改变，表明CFA处理的KK-Ay小鼠的能量消耗增加。为了观察能量消耗的增加，测量CFA处理和对照小鼠的体温、耗氧量和心率。然而，两组之间的这些测量值没有显著差异。在C57/BL小鼠和KK-Ay小鼠中检测UCP-2和UCP-3的mRNA表达。KK-Ay小鼠脾脏、白色脂肪组织和肌肉中UCP-2 mRNA的表达有低于C57/BL小鼠的趋势，CFA处理后这些表达增加。正在进行进一步的实验以证实这些结果。最后，对肥胖2型糖尿病患者进行餐前、餐后鼓膜温度检测，以筛查能量代谢异常。但由于体温变化不稳定，范围较广，未发现明显异常的患者。

Expression of UCP-2 and UCP-3 genes in obese type 2 diabetes mellitus and its modification by a cytokine inducerKK-Ay mouse is a model of obese type 2 diabetes mellitus. Glucose intolerance of KK-Ay mice was significantly improved by CFA treatment and the improvement was medicated by IL-1. CFA-treated KK-Ay mice lost body weight as compared to saline-treated control mice even though food intake was not changed, suggesting increase of energy expenditure in CFA-treated KK-Ay mice. To observe the increase of energy expenditure, body temperature, oxygen consumption and heart rate were measured in CFA-treated and control mice. However, there was no significant different in these measurements between both groups. mRNA expression of UCP-2 and UCP-3 was examined in C57/BL mice and KK-Ay mice. There was a tendency that expression of UCP-2 mRNA in the spleen, white adipose tissue and muscle were lower in KK-Ay mice than those in C57/BL mice and these were increased by CFA treatment. Further experiments were in progress to confirm these results. Finally, to screen obese patients with type 2 diabetes mellitus for abnormal energy metabolism, we measured temperature of tympanitic membrane before and after meals. However, we could not find obviously abnormal patients in the temperature change, because of unstable changes with wide range.