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Submitted on June 8, 2005
Accepted on October 26, 2005
Division of Division of Diabetes, Endocrinology and Metabolism, Section of Atherosclerosis and Lipoprotein Research, and Section of Pulmonary and Critical Care Medicine, Department of Medicine, Section of Nutrition and Section of Leukocyte Biology, Department of Pediatrics, and Division of General Surgery, Department of Surgery, Baylor College of Medicine; and Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart Center, Houston, TX
* To whom correspondence should be addressed. E-mail: cmb{at}bcm.tmc.edu.
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. To examine the relation between eotaxin and obesity.
Design. Comparison of eotaxin in mice fed high-fat vs. standard chow diet for 26 weeks, in obese vs. lean humans, in obese humans before and after 4-6 weeks of weight loss, and in sc vs. visceral adipose tissue from patients undergoing bariatric surgery.
Setting. Outpatient weight loss program.
Patients. Obese adults with metabolic syndrome (n = 40) and 9 morbidly obese bariatric surgery patients.
Intervention. Very low calorie diet
Main Outcome Measures. 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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