Department of Molecular Genetics, Institute of Life Science, Kurume University, 1-1 Hyakunen-kouen, Kurume 839-0864, Japan.
Biochem Biophys Res Commun. 2013 Nov 8;441(1):42-6. doi: 10.1016/j.bbrc.2013.10.014. Epub 2013 Oct 12.
Cold exposure and β3-adrenergic receptor agonist (CL316,243) treatment induce the production of beige cells, which express brown adipocytes(BA)-specific UCP1 protein, in white adipose tissue (WAT). It remains unclear whether the beige cells, which have different gene expression patterns from BA, express BA-characteristic fatty acid oxidation (FAO) proteins. Here we found that 5 day cold exposure and CL316,243 treatment of WAT, but not CL316,243 treatment of primary adipocytes of C57BL/6J mice, increased mRNA levels of BA-characteristic FAO proteins. These results suggest that BA-characteristic FAO proteins are induced in beige cells in a different pathway from UCP1.
冷暴露和β3-肾上腺素能受体激动剂(CL316,243)治疗可诱导白色脂肪组织(WAT)中产生表达棕色脂肪细胞(BA)特异性 UCP1 蛋白的米色细胞。目前尚不清楚这些与 BA 具有不同基因表达模式的米色细胞是否表达 BA 特征性的脂肪酸氧化(FAO)蛋白。在这里,我们发现 5 天的冷暴露和 CL316,243 处理 WAT,但不是 CL316,243 处理 C57BL/6J 小鼠的原代脂肪细胞,可增加 BA 特征性 FAO 蛋白的 mRNA 水平。这些结果表明,BA 特征性 FAO 蛋白在米色细胞中的诱导途径与 UCP1 不同。