自备抗血清采用酶联免疫法测定了中缅树鼩(Tupaia belangeri)在(5±1)℃冷暴露0 d、7 d、14 d、21d、28 d时,褐色脂肪组织(BAT)中解偶联蛋白1(UCP1)的含量。结果表明,随着冷暴露时间的延长,中缅树鼩的体重、褐色脂肪组织重量均表现出了增加的趋势,BAT线粒体总蛋白和UCP1的含量也呈增加的趋势,其中UCP1的含量在28 d时达到极显著水平,比对照组增加了55.9%。说明冷暴露能够诱导中缅树鼩UCP1表达增加,从而使其适应性产热增加。
Uncoupling proteins (UCPs) increase proton leakage across the inner mitochondrial membrane. UCP1 in brown adipose tissue dissipates proton motive force as heat. This mechanism of nonshivering thermogenesis is considered as a monophyletic trait of endothermic placental mammals and provided a crucial advantage for life in the cold. Thereby, UCP1 is thus the only protein capable of mediating cold-acclimation-recruited adaptive adrenergic nonshivering thermogenesis. In this study, the content of UCP1 in BAT in Tree Shrews ( Tupaia belangeri ) was measured during cold exposure for 0 day, 7 days, 21 days and 28 days by enzyme-linked immunosorbent assay. The body weight, BAT weight, mitochondrial protein contents and UCP1 contents greatly increased with the cold exposure. The UCP1 content increased by 55.9 % ( P 〈 O. O1 ) significantly after 28 days cold acclimation. The changes in BAT thermogenic properties are important for the survival under cold stress in T. belangeri.