Association Between Adiponectin and Mediators of Inflammation in Obese Women
- Stefan Engeli1,
- Mareike Feldpausch1,
- Kerstin Gorzelniak1,
- Frauke Hartwig1,
- Ute Heintze1,
- Jürgen Janke1,
- Matthias Möhlig2,
- Andreas F.H. Pfeiffer2,
- Friedrich C. Luft1 and
- Arya M. Sharma13
- 1HELIOS Klinikum Berlin, Franz Volhard Clinic, Medical Faculty of the Charité, Humboldt University of Berlin, and Max Delbrück Center for Molecular Medicine, Berlin, Germany
- 2German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany
- 3Department of Internal Medicine, McMaster University, Hamilton, Ontario, Canada
Abstract
Low plasma levels of the anti-inflammatory factor adiponectin characterize obesity and insulin resistance. To elucidate the relationship between plasma levels of adiponectin, adiponectin gene expression in adipose tissue, and markers of inflammation, we obtained blood samples, anthropometric measures, and subcutaneous adipose tissue samples from 65 postmenopausal healthy women. Adiponectin plasma levels and adipose-tissue gene expression were significantly lower in obese subjects and inversely correlated with obesity-associated variables, including high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6). Despite adjustment for obesity-associated variables, plasma levels of adiponectin were significantly correlated to adiponectin gene expression (partial r = 0.38, P < 0.05). Furthermore, the inverse correlation between plasma levels of hs-CRP and plasma adiponectin remained significant despite correction for obesity-associated variables (partial r = −0.32, P < 0.05), whereas the inverse correlation between adiponectin plasma levels or adiponectin gene expression in adipose tissue with plasma IL-6 were largely dependent on the clustering of obesity-associated variables. In conclusion, our data suggest a transcriptional mechanism leading to decreased adiponectin plasma levels in obese women and demonstrate that low levels of adiponectin are associated with higher levels of hs-CRP and IL-6, two inflammatory mediators and markers of increased cardiovascular risk.
Footnotes
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Address correspondence and reprint requests to Stefan Engeli, MD, Franz-Volhard-Klinik, Wiltberg Strasse 50, 13125 Berlin, Germany. E-mail: engeli{at}fvk.charite-buch.de.
Received for publication 13 August 2002 and accepted in revised form 2 January 2003.
CRP, C-reactive protein; CV, coefficient of variation; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; HOMA, homeostasis model assessment; hs-CRP, high-sensitive CRP; IL-6, interleukin-6; NF, nuclear factor; TNF-α, tumor necrosis factor-α.
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