title: Hypoadiponectinemia and proinflammatory state: two sides of the same coin?: results from the Cooperative Health Research in the Region of Augsburg Survey 4 (KORA S4).
abstract: OBJECTIVE
  Previous studies have yielded conflicting results on the association of adiponectin levels and inflammation. Low systemic concentrations of adiponectin, as well as elevated levels of immune mediators, represent risk factors for the development of type 2 diabetes and coronary artery disease. The major aim of this cross-sectional study was to investigate the interdependence of hypoadiponectinemia and low-grade systemic inflammation.
  
  
  METHODS
  The study sample consisted of 606 participants aged 55-74 years (244 with normal glucose tolerance, 242 with impaired glucose tolerance, and 120 with newly diagnosed type 2 diabetes) of the population-based KORA S4 (Cooperative Health Research in the Region of Augsburg Survey 4; 1999-2001). Systemic concentrations of adiponectin and a wide range of anthropometric, metabolic, and inflammatory variables were available for analyses. The association of adiponectin with 15 immunological markers, including leukocyte count, acute-phase proteins, cytokines, cytokine receptors, and chemokines, was assessed using univariable and multivariable models.
  
  
  RESULTS
  No evidence for a significant correlation between adiponectin and all immunological parameters except eotaxin could be found after multivariable adjustments, whereas multiple strong correlations with obesity and metabolic factors were present.
  
  
  CONCLUSIONS
  From these data, we conclude that hypoadiponectinemia and a proinflammatory state are largely independent from each other.
authors.affiliation: German Diabetes Clinic, German Diabetes Center, Leibniz Center at Heinrich Heine University, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany. christian.herder@ddz.uni-duesseldorf.de
authors.forename: Christian
authors.initials: C
authors.lastname: Herder
authors.forename: Hans
authors.initials: H
authors.lastname: Hauner
authors.forename: Burkhard
authors.initials: B
authors.lastname: Haastert
authors.forename: Karin
authors.initials: K
authors.lastname: Röhrig
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Koenig
authors.forename: Hubert
authors.initials: H
authors.lastname: Kolb
authors.forename: Sylvia
authors.initials: S
authors.lastname: Müller-Scholze
authors.forename: Barbara
authors.initials: B
authors.lastname: Thorand
authors.forename: Rolf
authors.initials: R
authors.lastname: Holle
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rathmann
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000368:Aged; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000097:blood; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000503:physiopathology; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D052242:Adiponectin; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha