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CD137 negatively affects “browning” of white adipose tissue during cold exposure

机译:CD137在冷暴露过程中对白色脂肪组织的“褐变”产生负面影响

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Prolonged cold exposure stimulates the formation of brownlike adipocytes expressing UCP1 (uncoupling-protein-1) in subcutaneous white adipose tissue which, together with classical brown adipose tissue, contributes to maintaining body temperature in mammals through nonshivering thermogenesis. The mechanisms that regulate the formation of these cells, alternatively called beige or brite adipocytes, are incompletely understood. Here we report that mice lacking CD137, a cell surface protein used in several studies as a marker for beige adipocytes, showed elevated levels of thermogenic markers, including UCP1, increased numbers of beige adipocyte precursors, and expanded UCP1-expressing cell clusters in inguinal white adipose tissue after chronic cold exposure. CD137 knockout mice also showed enhanced cold resistance. These results indicate that CD137 functions as a negative regulator of “browning” in white adipose tissue and call into question the use of this protein as a functional marker for beige adipocytes.
机译:延长的冷曝光刺激在皮下白色脂肪组织中表达UCP1(Uncuping-Prote-1)的棕状脂肪细胞的形成,该组织与古典棕色脂肪组织一起有助于通过不发热的热生成保持哺乳动物的体温。调节这些细胞的形成的机制,或者称为米色或背骨脂肪细胞,被不完全理解。在这里,我们报告缺乏CD137的小鼠,其中几种研究中使用的细胞表面蛋白作为米色脂肪细胞的标志物,显示出升高的热标记物水平,包括UCP1,米色脂肪细胞前体的数量增加,并且在腹股沟上扩展了UCP1表达的细胞簇。慢性冷暴露后脂肪组织。 CD137敲除小鼠还显示出增强的耐寒性。这些结果表明CD137用作白色脂肪组织中的“褐变”的负调节器,并调用该蛋白质作为米色脂肪细胞的功能标志物的用途。

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