Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Genes Dev. 2010 Feb 1;24(3):256-64. doi: 10.1101/gad.1878510. Epub 2010 Jan 15.
The cJun N-terminal kinase 1 (JNK1) is implicated in diet-induced obesity. Indeed, germline ablation of the murine Jnk1 gene prevents diet-induced obesity. Here we demonstrate that selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. The failure to increase body mass is mediated, in part, by increased energy expenditure that is associated with activation of the hypothalamic-pituitary-thyroid axis. Disruption of thyroid hormone function prevents the effects of nervous system JNK1 deficiency on body mass. These data demonstrate that the hypothalamic-pituitary-thyroid axis represents an important target of metabolic signaling by JNK1.
cJun N-末端激酶 1（JNK1）与饮食诱导的肥胖有关。事实上，敲除小鼠 Jnk1 基因可预防饮食诱导的肥胖。在这里，我们证明了选择性敲除小鼠神经系统中的 JNK1 足以抑制饮食诱导的肥胖。体重增加的失败部分是由于能量消耗增加所致，这与下丘脑-垂体-甲状腺轴的激活有关。甲状腺激素功能的破坏阻止了神经系统 JNK1 缺乏对体重的影响。这些数据表明，下丘脑-垂体-甲状腺轴是 JNK1 代谢信号的一个重要靶点。
