Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1

被引:90
作者
Sabio, Guadalupe [1 ,2 ]
Cavanagh-Kyros, Julie [1 ,2 ]
Barrett, Tamera [1 ,2 ]
Jung, Dae Young [2 ,3 ]
Ko, Hwi Jin [2 ,3 ]
Ong, Helena [2 ]
Morel, Caroline [1 ,2 ]
Mora, Alfonso [2 ]
Reilly, Judith [2 ]
Kim, Jason K. [2 ,3 ,4 ]
Davis, Roger J. [1 ,2 ]
机构
[1] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
[2] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA
[3] Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA
[4] Univ Massachusetts, Sch Med, Dept Med, Div Endocrinol Metab & Diabet, Worcester, MA 01605 USA
基金
美国国家卫生研究院;
关键词
JNK1; obesity; insulin resistance; thyroid hormone; INSULIN-RESISTANCE; PATHWAY; OBESITY; GENE;
D O I
10.1101/gad.1878510
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:256 / 264
页数:9
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