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在aP2-Ucp小鼠中,棕色脂肪对于冷诱导产热至关重要,但对于抗肥胖作用并非必需。

Brown fat is essential for cold-induced thermogenesis but not for obesity resistance in aP2-Ucp mice.

作者信息

Stefl B, Janovská A, Hodný Z, Rossmeisl M, Horáková M, Syrový I, Bémová J, Bendlová B, Kopecký J

机构信息

Faculty of Sciences, Charles University, Prague, Czech Republic.

出版信息

Am J Physiol. 1998 Mar;274(3):E527-33. doi: 10.1152/ajpendo.1998.274.3.E527.

DOI:10.1152/ajpendo.1998.274.3.E527
PMID:9530137
Abstract

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.

摘要

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C57BL6/J同窝小鼠。转基因动物对高脂饮食诱导的肥胖具有抗性,这可能是由于白色脂肪中UCP-1的异位合成。这些动物表现出棕色脂肪组织萎缩,表现为棕色脂肪体积较小,其总UCP-1和DNA含量降低。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)与转基因剂量成比例降低,纯合(而非杂合)转基因小鼠在寒冷中维持体温的能力降低。我们的结果表明,棕色脂肪在冷诱导产热中的作用不能被其他组织增加的能量消耗所替代。

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Brown fat is essential for cold-induced thermogenesis but not for obesity resistance in aP2-Ucp mice.在aP2-Ucp小鼠中,棕色脂肪对于冷诱导产热至关重要,但对于抗肥胖作用并非必需。
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