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Eotaxin and obesity.

Abu R Vasudevan1, Huaizhu Wu, Antonios M Xydakis

  • 1Division of Diabetes, Endocrinology, and Metabolism, Baylor College of Medicine, Houston, Texas 77030, USA.

The Journal of Clinical Endocrinology and Metabolism
|November 3, 2005
PubMed
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Obesity increases eotaxin, a key inflammatory chemokine, in both mice and humans. Weight loss interventions effectively reduce these elevated eotaxin levels, highlighting a link between obesity and inflammation.

Area of Science:

  • Immunology and Metabolism
  • Inflammatory Chemokines and Obesity Research

Background:

  • Global increases in asthma and obesity incidence are observed.
  • Asthma severity is often exacerbated in individuals with obesity.
  • Eotaxin, a CC chemokine, plays a role in extrinsic asthma pathogenesis.

Purpose of the Study:

  • To investigate the relationship between eotaxin and obesity.
  • To determine if obesity influences eotaxin levels in animal models and humans.

Main Methods:

  • Comparative study in mice on high-fat vs. standard diets.
  • Analysis of obese vs. lean humans, including pre- and post-weight loss.
  • Assessment of eotaxin and eotaxin mRNA in subcutaneous (sc) vs. visceral adipose tissue from bariatric surgery patients.

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Main Results:

  • Obese mice and humans exhibited significantly higher serum/plasma eotaxin levels compared to lean counterparts.
  • Adipose tissue explants from obese mice secreted more eotaxin.
  • Eotaxin mRNA levels were substantially higher in visceral adipose tissue.
  • Diet-induced weight loss in humans led to a significant reduction in plasma eotaxin.

Conclusions:

  • Obesity is associated with increased circulating eotaxin and adipose tissue eotaxin mRNA.
  • Adipose tissue, particularly the stromal/vascular component, is a significant source of eotaxin.
  • Clinical interventions targeting obesity can effectively modulate systemic eotaxin levels.