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Genes Dev. 2010 Feb 1;24(3):256-64. doi: 10.1101/gad.1878510. Epub 2010 Jan 15.

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

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1
Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.

Abstract

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.

PMID:
20080940
PMCID:
PMC2811827
DOI:
10.1101/gad.1878510
[Indexed for MEDLINE]
Free PMC Article
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