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A central role for JNK in obesity and insulin resistance

Jiro Hirosumi1, Gürol Tuncman, Lufen Chang

  • 1Division of Biological Sciences and Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115, USA.

Nature
|November 26, 2002
PubMed

Insights

Obesity increases insulin resistance, a risk factor for type 2 diabetes. Blocking c-Jun amino-terminal kinases (JNK) reduced obesity and improved insulin sensitivity in mice, suggesting JNK as a therapeutic target.

Area of Science:

  • Biochemistry
  • Metabolic disease research
  • Molecular biology

Background:

  • Obesity is a major risk factor for type 2 diabetes mellitus, linked to insulin resistance.
  • The molecular mechanisms connecting obesity and insulin resistance are not fully understood.
  • c-Jun amino-terminal kinases (JNK) are implicated in insulin resistance and activated by inflammatory molecules relevant to diabetes.

Purpose of the Study:

  • To investigate the role of JNK activity in obesity-induced insulin resistance.
  • To determine if JNK is a potential therapeutic target for obesity and type 2 diabetes.

Main Methods:

  • Measuring JNK activity in obese models.
  • Analyzing the effects of JNK1 absence on adiposity and insulin sensitivity in mouse models of obesity.

Main Results:

  • JNK activity was found to be abnormally elevated in obesity.
  • Mice lacking JNK1 exhibited reduced adiposity and significantly improved insulin sensitivity.
  • Insulin receptor signaling capacity was enhanced in JNK1-deficient obese mice.

Conclusions:

  • JNK plays a critical role in mediating obesity and insulin resistance.
  • JNK inhibition represents a promising therapeutic strategy for managing obesity and type 2 diabetes.

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