Disclosure: The authors declare that there is no conflict of interest.
The Macrophage-Specific Serum Marker, Soluble CD163, Is Increased in Obesity and Reduced After Dietary-Induced Weight Loss
Article first published online: 1 JUL 2013
Copyright © 2013 The Obesity Society
Volume 21, Issue 12, pages 2437–2443, December 2013
How to Cite
Fjeldborg, K., Christiansen, T., Bennetzen, M., J. Møller, H., Pedersen, S. B. and Richelsen, B. (2013), The Macrophage-Specific Serum Marker, Soluble CD163, Is Increased in Obesity and Reduced After Dietary-Induced Weight Loss. Obesity, 21: 2437–2443. doi: 10.1002/oby.20376
Funding agencies: This study was supported by Aarhus University, Novo Nordic Foundation, and the Danish Agency for Strategic Research (TRAIN project).
- Issue published online: 3 DEC 2013
- Article first published online: 1 JUL 2013
- Accepted manuscript online: 20 MAR 2013 02:08AM EST
- Manuscript Accepted: 26 DEC 2012
- Manuscript Received: 11 OCT 2012
- Aarhus University
- Novo Nordic Foundation
- Strategic Research (TRAIN project)
Objective: Soluble CD163 (sCD163) is a new macrophage-specific serum marker elevated in inflammatory conditions. sCD163 is elevated in obesity and found to be a strong predictor of the development of type 2 diabetes. We investigated whether dietary intervention and moderate exercise was related to changes in sCD163 and how sCD163 is associated to insulin resistance in obesity.
Design and Methods: Ninety-six obese subjects were enrolled: 62 followed a very low energy diet (VLED) program for 8 weeks followed by 3-4 weeks of weight stabilization, 20 followed a moderate exercise program for 12 weeks, and 14 were included without any intervention. Fasting blood samples and anthropometric measures were taken at baseline and after intervention. Thirty-six lean subjects were included in a control group.
Results: sCD163 was significantly higher in obese subjects (2.3 ± 1.0 mg/l) compared with lean (1.6 ± 0.4 mg/l, P < 0.001). Weight loss (11%) induced by VLED resulted in a reduction and partial normalization of sCD163 to 2.0 ± 0.9 mg/l (P < 0.001). Exercise for 12 weeks had no effect on sCD163. At baseline, sCD163 was significantly correlated with BMI (r = 0.46), waist circumference (r = 0.40), insulin resistance measured by the homeostasis model assessment (HOMA-IR; r = 0.41; all P < 0.001), and the leptin-to-adiponectin ratio (r = 0.28, P < 0.05). In a multivariate linear regression analysis with various inflammatory markers, sCD163 (β = 0.25), adiponectin (β = −0.24), and high sensitivity C-reactive protein (hs-CRP; β = 0.20) remained independently and significantly associated to HOMA-IR (all P < 0.05). After further adjustment for waist circumference, only sCD163 was associated with HOMA-IR (P < 0.05).
Conclusion: The macrophage-specific serum marker sCD163 is increased in obesity and partially normalized by dietary-induced weight loss but not by moderate exercise. Furthermore, we confirm that sCD163 is a good marker for obesity-related insulin resistance.