Program in Molecular Medicine
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
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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DOI of Published Version
Genes Dev. 2010 Feb 1;24(3):256-64. doi: 10.1101/gad.1878510. Epub 2010 Jan 15. Link to article on publisher's site
Genes and development
Sabio G, Cavanagh-Kyros J, Barrett T, Jung D, Ko HJ, Ong H, Morel C, Mora A, Reilly J, Kim JK, Davis RJ. (2010). Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1. Davis Lab Publications. https://doi.org/10.1101/gad.1878510. Retrieved from https://escholarship.umassmed.edu/davis/80
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