Adiponectin is a mediator of the inverse association of adiposity with radiographic damage in rheumatoid arthritis
Version of Record online: 27 AUG 2009
Copyright © 2009 by the American College of Rheumatology
Arthritis Care & Research
Volume 61, Issue 9, pages 1248–1256, 15 September 2009
How to Cite
Giles, J. T., Allison, M., Bingham, C. O., Scott, W. M. and Bathon, J. M. (2009), Adiponectin is a mediator of the inverse association of adiposity with radiographic damage in rheumatoid arthritis. Arthritis & Rheumatism, 61: 1248–1256. doi: 10.1002/art.24789
- Issue online: 27 AUG 2009
- Version of Record online: 27 AUG 2009
- Manuscript Accepted: 8 JUN 2009
- Manuscript Received: 3 FEB 2009
- Unknown funding agency. Grant Number: M01-RR02719
- National Institute of Arthritis and Musculoskeletal and Skin Diseases of the NIH. Grant Number: 1-K23-AR054112-01
- Clinical Investigator Fellowship award from the American College of Rheumatology Research and Education Foundation
- Institutional grant and a Chapter grant from the Arthritis Foundation Maryland Chapter
- National Institute of Arthritis and Musculoskeletal and Skin Diseases of the NIH. Grant Number: AR050026-01
- American College of Rheumatology Research and Education Foundation
Recent reports have suggested that increasing adiposity may protect against radiographic damage in rheumatoid arthritis (RA). We explored the role of serum adipokines (adiponectin, resistin, and leptin) in mediating this association.
Patients with RA underwent total-body dual x-ray absorptiometry for measurement of total and regional body fat and lean mass, abdominal computed tomography for measurement of visceral fat area, and radiographs of the hands and feet scored according to the modified Sharp/van der Heijde (SHS) method. Serum levels of adipokines were measured and cross-sectional associations with radiographic damage were explored, adjusting for pertinent confounders. The associations of measures of adiposity with radiographic damage were explored with the introduction of adipokines into multivariable modeling as potential mediators.
Among the 197 patients studied, adiponectin demonstrated a strong association with radiographic damage, with the log SHS score increasing by 0.40 units for each log unit increase in adiponectin (P = 0.001) after adjusting for pertinent predictors of radiographic damage. Adiponectin independently accounted for 6.1% of the explainable variability in SHS score, a proportion comparable with rheumatoid factor, and greater than HLA–DRB1 shared epitope alleles or C-reactive protein levels. Resistin and leptin were not associated with radiographic damage in adjusted models. An inverse association between visceral fat area and radiographic damage was attenuated when adiponectin was modeled as a mediator. The association of adiponectin with radiographic damage was stronger in patients with longer disease duration.
Adiponectin may represent a mechanistic link between low adiposity and increased radiographic damage in RA. Adiponectin modulation may represent a novel strategy for attenuating articular damage.