Brown fat is essential for cold-induced thermogenesis but not for obesity resistance in aP2-Ucp mice
Brown fat is essential for cold-induced thermogenesis but not for obesity resistance in aP2-Ucp mice
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DOI：
10.1152/ajpendo.1998.274.3.e527
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发表时间：
1998-03-01
影响因子：
5.1
通讯作者：
Kopecky, J
中科院分区：
文献类型：
--
作者：
Stefl, B;Janovská, A;Kopecky, J
研究了棕色脂肪组织在总能量平衡和冷诱导产热中的作用。使用了从脂肪特异性aP2基因启动子表达线粒体解偶联蛋白1（UCP-1）的小鼠（杂合和纯合aP2-Ucp转基因小鼠）及其非转基因C57 BL 6/J同窝小鼠。转基因动物对高脂饮食诱导的肥胖有抵抗力，这可能是由于UCP-1在白色脂肪中的异位合成。这些动物表现出棕色脂肪组织萎缩，如棕色脂肪尺寸较小及其总UCP-1和DNA含量降低所示。去甲肾上腺素诱导的呼吸（在戊巴比妥钠麻醉的动物中测量）与转基因的剂量成比例地降低，纯合（但不是杂合）转基因小鼠在寒冷中保持体温的能力降低。我们的研究结果表明，棕色脂肪在冷诱导产热中的作用不能被其他组织中能量消耗的增加所取代。
The role of brown adipose tissue in total energy balance and cold-induced thermogenesis was studied. Mice expressing mitochondrial uncoupling protein 1 (UCP-1) from the fat-specific aP2 gene promoter (heterozygous and homozygous aP2-Ucp transgenic mice) and their nontransgenic C57BL6/J littermates were used. The transgenic animals are resistant to obesity induced by a high-fat diet, presumably due to ectopic synthesis of UCP-1 in white fat. These animals exhibited atrophy of brown adipose tissue, as indicated by smaller size of brown fat and reduction of its total UCP-1 and DNA contents. Norepinephrine-induced respiration (measured in pentobarbital sodium-anesthetized animals) was decreased proportionally to the dosage of the transgene, and the homozygous (but not heterozygous) transgenic mice exhibited a reduction in their capacity to maintain body temperature in the cold. Our results indicate that the role of brown fat in cold-induced thermogenesis cannot be substituted by increased energy expenditure in other tissues.