期刊
GENES & DEVELOPMENT
卷 24, 期 3, 页码 256-264出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1878510
关键词
JNK1; obesity; insulin resistance; thyroid hormone
资金
- National Institutes of Health [CA65861, DK80756]
- American Diabetes Association [7-07-RA-80]
- University of Massachusetts Mouse Phenotyping Center (National Institute of Diabetes and Digestive and Kidney Diseases, Diabetes and Endocrinology Research Center) [DK52530]
- Penn State Diabetes and Obesity Mouse Phenotyping Center
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.
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