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

Santiago Vernia1, Julie Cavanagh-Kyros, Tamera Barrett

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

Genes & Development
|November 5, 2013
PubMed

Insights

The cJun N-terminal kinase (JNK) pathway impacts obesity. Blocking JNK in the pituitary reduced obesity by increasing thyroid hormone, boosting energy expenditure.

Area of Science:

  • Endocrinology
  • Metabolic signaling
  • Obesity research

Background:

  • The cJun N-terminal kinase (JNK) signaling pathway is implicated in metabolic stress and obesity development.
  • High-fat diets trigger JNK activation, contributing to metabolic dysfunction.

Purpose of the Study:

  • To investigate the role of JNK signaling in the anterior pituitary gland in diet-induced obesity.
  • To elucidate the molecular mechanisms linking JNK, thyroid hormones, and energy expenditure.

Main Methods:

  • Targeted ablation of Jnk genes in the anterior pituitary of mice.
  • Analysis of thyroid-stimulating hormone (TSH) and thyroid hormone (T4) levels.
  • Assessment of energy expenditure and obesity development.

Main Results:

  • Mice with JNK-deficient pituitaries showed increased pituitary TSH and blood T4 concentrations.
  • These mice exhibited significantly reduced obesity and increased energy expenditure.
  • Reduced expression of type 2 iodothyronine deiodinase (Dio2) in the pituitary was observed, impairing negative feedback.

Conclusions:

  • JNK signaling in the anterior pituitary regulates energy expenditure and obesity.
  • A novel mechanism involving JNK, Dio2, and thyroid hormone feedback controls metabolic adaptation to high-fat diets.
Keywords:
DIO2JNKobesitypituitary glandthyroid hormone

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