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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Publisher PDF posted as allowed by the publisher's author rights policy at http://genesdev.cshlp.org/site/misc/terms.xhtml. Citation: 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.
Sabio, Guadalupe; Cavanagh-Kyros, Julie; Barrett, Tamera; Jung, Dae Young; Ko, Hwi Jin; Ong, Helena; Morel, Caroline; Mora, Alfonso; Reilly, Judith; Kim, Jason K.; and Davis, Roger J., "Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1" (2010). Davis Lab. 80.
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