Format

Send to

Choose Destination
See comment in PubMed Commons below
Genes Dev. 2013 Nov 1;27(21):2345-55. doi: 10.1101/gad.223800.113.

Diet-induced obesity mediated by the JNK/DIO2 signal transduction pathway.

Author information

1
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA;

Abstract

The cJun N-terminal kinase (JNK) signaling pathway is a key mediator of metabolic stress responses caused by consuming a high-fat diet, including the development of obesity. To test the role of JNK, we examined diet-induced obesity in mice with targeted ablation of Jnk genes in the anterior pituitary gland. These mice exhibited an increase in the pituitary expression of thyroid-stimulating hormone (TSH), an increase in the blood concentration of thyroid hormone (T4), increased energy expenditure, and markedly reduced obesity compared with control mice. The increased amount of pituitary TSH was caused by reduced expression of type 2 iodothyronine deiodinase (Dio2), a gene that is required for T4-mediated negative feedback regulation of TSH expression. These data establish a molecular mechanism that accounts for the regulation of energy expenditure and the development of obesity by the JNK signaling pathway.

KEYWORDS:

DIO2; JNK; obesity; pituitary gland; thyroid hormone

PMID:
24186979
PMCID:
PMC3828520
DOI:
10.1101/gad.223800.113
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center