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

AuthorsSabio, Guadalupe; Cavanagh-Kyros, Julie; Barrett, Tamera; Young Jung, Dae; Jin Ko, Hwi; Ong, Helena; Morel, Caroline; Mora, Alfonso; Reilly, Judith; Kim, Jason K.; Davis, Roger J.
Insulin resistance
Thyroid hormone
Issue Date15-Jan-2010
PublisherCold Spring Harbor Laboratory Press
CitationGenes & Development 24(2): (2010)
AbstractThe 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.
Publisher version (URL)http://dx.doi.org/10.1101/gad.1878510
Appears in Collections:(CNB) Artículos
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