一项研究说，褐色脂肪会响应神经系统感知到的寒冷温度从而把化学能转化成热，而与褐色脂肪不同，一小组白色脂肪细胞能够直接感知温度的变化，从而激活参与产热的基因。为了帮助人体在冷环境中维持体温，神经系统通过激活脂肪细胞中的β-肾上腺素受体（β-AR）从而在褐色脂肪中刺激产热或生热作用。Bruce Spiegelman及其同事发现，尽管缺乏β-肾上腺素受体（β-AR）的小鼠的褐色脂肪的生热作用被削弱，在暴露于寒冷之中的时候，这些动物显示出了皮肤下面的白色皮下脂肪层的产热基因的表达增加，这提示皮下脂肪细胞可能通过一个与β-肾上腺素受体（β-AR）无关的路径调控产热。为了确定皮下脂肪细胞是否直接感受环境温度，这组作者让培养的脂肪细胞暴露在27到39摄氏度之间的温度中，结果发现了33摄氏度以下的温度诱导了白色和米色脂肪细胞中的产热基因的表达，但是没有在褐色脂肪细胞中发现该表达。此外，对这些基因表达的诱发与β-肾上腺素受体（β-AR）以及在褐色脂肪中调控产热作用的其他蛋白无关。这组作者说，这些发现提示温度可能直接在某些脂肪细胞中刺激产热。（生物谷 Bioon.com）
生物谷推荐的英文摘要
PNAS doi: 10.1073/pnas.1310261110
Fat cells directly sense temperature to activate thermogenesis
Li Yea,b, Jun Wua,b, Paul Cohena,b, Lawrence Kazaka,b, Melin J. Khandekara,b, Mark P. Jedrychowskib, Xing Zenga,b, Steven P. Gygib, and Bruce M. Spiegelman
Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1. This nonshivering thermogenesis is crucial for mammals as a defense against cold and obesity/diabetes. Cold is known to act indirectly through the sympathetic nervous systems and β-adrenergic signaling, but here we report that cool temperature (27–33 °C) can directly activate a thermogenic gene program in adipocytes in a cell-autonomous manner. White and beige fat cells respond to cool temperatures, but classic brown fat cells do not. Importantly, this activation in isolated cells is independent of the canonical cAMP/Protein Kinase A/cAMP response element-binding protein pathway downstream of the β-adrenergic receptors. These findings provide an unusual insight into the role of adipose tissues in thermoregulation, as well as an alternative way to target nonshivering thermogenesis for treatment of obesity and metabolic diseases.
