title: Reduction of inflammatory cytokine concentrations and improvement of endothelial functions in obese women after weight loss over one year.
abstract: BACKGROUND
  Visceral fat is a key regulator site for the process of inflammation, and atherosclerotic lesions are essentially an inflammatory response.
  
  
  RESULTS
  Fifty-six healthy premenopausal obese women (age range 25 to 44 years, body mass index 37.2+/-2.2, waist to hip ratio range 0.78 to 0.92) and 40 age-matched normal weight women were studied. Compared with nonobese women, obese women had increased basal concentrations of tumor necrosis factor-alpha (TNF-alpha, P<0.01), interleukin-6 (IL-6, P<0.01), P-selectin (P<0.01), intercellular adhesion molecule-1 (ICAM-1, P<0.02), and vascular adhesion molecule-1 (VCAM-1, P<0.05). Vascular responses to L-arginine (3 g IV), the natural precursor of nitric oxide, were impaired in obese women: reductions in mean blood pressure (P<0.02), platelet aggregation to adenosine diphosphate (P<0.05), and blood viscosity (P<0.05) were significantly lower as compared with those in the nonobese group. Concentrations of TNF-alpha and IL-6 were related (P<0.01) to visceral obesity, as well as to adhesin levels and responses to L-arginine. After 1 year of a multidisciplinary program of weight reduction (diet, exercise, behavioral counseling), all obese women lost at least 10% of their original weight (9.8+/-1.5 kg, range 7.5 to 13 kg). Compared with baseline, sustained weight loss was associated with reduction of cytokine (P<0.01) and adhesin (P<0.02) concentrations and with improvement of vascular responses to L-arginine.
  
  
  CONCLUSIONS
  In obese women, endothelial activation correlates with visceral body fat, possibly through inappropriate secretion of cytokines. Weight loss represents a safe method for downregulating the inflammatory state and ameliorating endothelial dysfunction in obese women.
authors.affiliation: Department of Geriatrics and Metabolic Diseases, Chair of Metabolic Diseases, Second University of Naples, Italy.
authors.forename: Patrizia
authors.initials: P
authors.lastname: Ziccardi
authors.forename: Francesco
authors.initials: F
authors.lastname: Nappo
authors.forename: Giovanni
authors.initials: G
authors.lastname: Giugliano
authors.forename: Katherine
authors.initials: K
authors.lastname: Esposito
authors.forename: Raffaele
authors.initials: R
authors.lastname: Marfella
authors.forename: Michele
authors.initials: M
authors.lastname: Cioffi
authors.forename: Francesco
authors.initials: F
authors.lastname: D'Andrea
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Molinari
authors.forename: Dario
authors.initials: D
authors.lastname: Giugliano
mesh_terms: D000328:Adult; D001120:Arginine / Q000494:pharmacology; D001786:Blood Glucose; D001824:Body Constitution; D015992:Body Mass Index; D016207:Cytokines / Q000097:blood*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007328:Insulin / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D015187:Lipectomy; D009765:Obesity / Q000178:diet therapy / Q000503:physiopathology* / Q000601:surgery; D019007:P-Selectin / Q000097:blood; D010974:Platelet Aggregation; D017697:Premenopause; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology; D015431:Weight Loss; D044465:White People
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D018836:Inflammation Mediators; D007328:Insulin; D015850:Interleukin-6; D019007:P-Selectin; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D001120:Arginine