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Herder, C.* ; Hauner, H.* ; Haastert, B.* ; Röhrig, K.* ; König, W.* ; Kolb, H.* ; Müller-Scholze, S.* ; Thorand, B. ; Holle, R. ; Rathmann, W.*

Hypoadiponectinemia and proinflammatory state: Two sides of the same coin?

Diabetes Care 29, 1626-1631 (2006)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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. RESEARCH DESIGN AND 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. © 2006 by the American Diabetes Association.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0149-5992
e-ISSN 1935-5548
Zeitschrift Diabetes Care
Quellenangaben Band: 29, Heft: 7, Seiten: 1626-1631 Artikelnummer: , Supplement: ,
Verlag American Diabetes Association
Verlagsort Alexandria, Va.
Begutachtungsstatus Peer reviewed