Literature DB >> 16263831

Eotaxin and obesity.

Abu R Vasudevan1, Huaizhu Wu, Antonios M Xydakis, Peter H Jones, E O'Brian Smith, John F Sweeney, David B Corry, Christie M Ballantyne.   

Abstract

CONTEXT: Asthma and obesity incidence is increasing worldwide, and asthma is often more severe in the obese. Eotaxin, a CC chemokine, is important in extrinsic asthma, an inflammatory disorder.
OBJECTIVE: Our objective was to examine the relation between eotaxin and obesity.
DESIGN: We conducted a comparison study of eotaxin in mice fed high-fat vs. standard chow diet for 26 wk, in obese vs. lean humans, in obese humans before and after 4-6 wk of weight loss, and in sc vs. visceral adipose tissue from patients undergoing bariatric surgery.
SETTING: Our clinical study occurred in an outpatient weight loss program. PATIENTS: Patients were obese adults with metabolic syndrome (n = 40) and nine morbidly obese bariatric surgery patients. INTERVENTION: Intervention was a very-low-calorie diet. MAIN OUTCOME MEASURES: We assessed circulating eotaxin and eotaxin mRNA levels in adipose tissue.
RESULTS: Serum eotaxin levels were significantly higher in obese mice, and adipose mRNA levels correlated positively with serum eotaxin levels. Adipose tissue explants from obese mice showed increased secretion of eotaxin compared with explants from lean mice. In obese patients, plasma eotaxin levels were significantly higher than in lean controls and significantly reduced after weight loss, and eotaxin mRNA levels were 4.7-fold higher in visceral than sc adipose tissue.
CONCLUSIONS: Circulating eotaxin and eotaxin mRNA levels in visceral adipose tissue were increased in obesity in mice and humans. Adipose tissue explants secrete eotaxin, and the stromal/vascular component of adipose tissue seems to be the predominant source of eotaxin. Diet-induced weight loss in humans led to reduction in plasma eotaxin levels, demonstrating that clinical interventions that target obesity can modulate systemic eotaxin levels.

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Year:  2005        PMID: 16263831     DOI: 10.1210/jc.2005-1280

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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