title: Eotaxin and obesity.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  Our clinical study occurred in an outpatient weight loss program.
  
  
  METHODS
  Patients were obese adults with metabolic syndrome (n = 40) and nine morbidly obese bariatric surgery patients.
  
  
  METHODS
  Intervention was a very-low-calorie diet.
  
  
  METHODS
  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.
authors.affiliation: Division of Diabetes, Endocrinology, and Metabolism, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Abu R
authors.initials: AR
authors.lastname: Vasudevan
authors.forename: Huaizhu
authors.initials: H
authors.lastname: Wu
authors.forename: Antonios M
authors.initials: AM
authors.lastname: Xydakis
authors.forename: Peter H
authors.initials: PH
authors.lastname: Jones
authors.forename: E O'Brian
authors.initials: EO
authors.lastname: Smith
authors.forename: John F
authors.initials: JF
authors.lastname: Sweeney
authors.forename: David B
authors.initials: DB
authors.lastname: Corry
authors.forename: Christie M
authors.initials: CM
authors.lastname: Ballantyne
mesh_terms: D016475:3T3 Cells; D017667:Adipocytes / Q000378:metabolism; D000273:Adipose Tissue / Q000737:chemistry / Q000378:metabolism; D000328:Adult; D000818:Animals; D001823:Body Composition / Q000502:physiology; D015992:Body Mass Index; D002454:Cell Differentiation; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000096:biosynthesis / Q000097:blood / Q000502:physiology*; D004032:Diet; D005260:Female; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism / Q000503:physiopathology*; D012313:RNA / Q000032:analysis; D013045:Species Specificity; D015431:Weight Loss / Q000502:physiology
chemical_list: C515456:CCL11 protein, human; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D012313:RNA