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Título

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

AutorSabio, 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.
Palabras claveJNK1
Obesity
Insulin resistance
Thyroid hormone
Fecha de publicación15-ene-2010
EditorCold Spring Harbor Laboratory. Press
CitaciónGenes & Development 24(2): (2010)
ResumenThe 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.
Versión del editorhttp://dx.doi.org/10.1101/gad.1878510
URIhttp://hdl.handle.net/10261/20551
DOI10.1101/gad.1878510
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