一項研究說,褐色脂肪會響應神經系統感知到的寒冷溫度從而把化學能轉化成熱,而與褐色脂肪不同,一小組白色脂肪細胞能夠直接感知溫度的變化,從而激活參與產熱的基因。為了幫助人體在冷環境中維持體溫,神經系統通過激活脂肪細胞中的β-腎上腺素受體(β-AR)從而在褐色脂肪中刺激產熱或生熱作用。Bruce Spiegelman及其同事發現,儘管缺乏β-腎上腺素受體(β-AR)的小鼠的褐色脂肪的生熱作用被削弱,在暴露於寒冷之中的時候,這些動物顯示出了皮膚下面的白色皮下脂肪層的產熱基因的表達增加,這提示皮下脂肪細胞可能通過一個與β-腎上腺素受體(β-AR)無關的路徑調控產熱。為了確定皮下脂肪細胞是否直接感受環境溫度,這組作者讓培養的脂肪細胞暴露在27到39攝氏度之間的溫度中,結果發現了33攝氏度以下的溫度誘導了白色和米色脂肪細胞中的產熱基因的表達,但是沒有在褐色脂肪細胞中發現該表達。此外,對這些基因表達的誘發與β-腎上腺素受體(β-AR)以及在褐色脂肪中調控產熱作用的其他蛋白無關。這組作者說,這些發現提示溫度可能直接在某些脂肪細胞中刺激產熱。(生物谷 Bioon.com)
生物谷推薦的英文摘要
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.