罗亚
cGMP依赖性蛋白激酶
褐色脂肪组织
细胞生物学
线粒体生物发生
产热
蛋白激酶A
蛋白激酶B
生物
脂肪生成
信号转导
线粒体
激酶
内分泌学
脂肪组织
丝裂原活化蛋白激酶激酶
间充质干细胞
作者
Bodo Haas,Péter Mayer,Katja Jennissen,Daniela Scholz,Mauricio Berriel Díaz,Wilhelm Bloch,Stephan Herzig,Reinhard Fässler,Alexander Pfeifer
出处
期刊:Science Signaling
[American Association for the Advancement of Science (AAAS)]
日期:2009-12-01
卷期号:2 (99)
被引量:125
标识
DOI:10.1126/scisignal.2000511
摘要
Brown adipose tissue (BAT) is a primary site of energy expenditure through thermogenesis, which is mediated by the uncoupling protein-1 (UCP-1) in mitochondria. Here, we show that protein kinase G (PKG) is essential for brown fat cell differentiation. Induction of adipogenic markers and fat storage was impaired in the absence of PKGI. Furthermore, PKGI mediated the ability of nitric oxide (NO) and guanosine 3',5'-monophosphate (cGMP) to induce mitochondrial biogenesis and increase the abundance of UCP-1. Mechanistically, we found that PKGI controlled insulin signaling in BAT by inhibiting the activity of RhoA and Rho-associated kinase (ROCK), thereby relieving the inhibitory effects of ROCK on insulin receptor substrate-1 and activating the downstream phosphoinositide 3-kinase-Akt cascade. Thus, PKGI links NO and cGMP signaling with the RhoA-ROCK and the insulin pathways, thereby controlling induction of adipogenic and thermogenic programs during brown fat cell differentiation.
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