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Research Article

Resistin is linked to inflammation, and leptin to metabolic syndrome, in women with inflammatory arthritis

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Pages 256-262 | Accepted 14 Dec 2011, Published online: 01 Apr 2011
 

Abstract

Objective: To investigate how inflammation and metabolic syndrome (MetS) are associated with adipokine levels in patients with inflammatory arthritis.

Methods: Fifty-four female patients with arthritis were enrolled in the study. Twenty (37%) of these patients had MetS, which was diagnosed according to the definition of the International Diabetes Federation (IDF). Interleukin (IL)-6 and four adipokines (resistin, leptin, adiponectin, and adipsin) were determined by immunoassay. Healthy women with body mass index (BMI) between 22 and 25 kg/m2 served as controls.

Results: The patients with arthritis had higher levels of resistin than the healthy controls. This difference was clear in patients without MetS (17.4 in patients vs. 10.8 ng/mL in controls, p < 0.001), and even higher resistin levels were found in the patients with MetS (20.7 ng/mL; p < 0.001 vs. healthy controls; and p = 0.095 vs. patients without MetS). In the patients with arthritis and MetS, resistin correlated positively with IL-6 (Pearson’s r = 0.5, p = 0.03). Leptin levels were increased in arthritis patients with MetS as compared to healthy controls, but not in patients without MetS. The statistically significant difference between patients with MetS and controls remained when leptin was adjusted with BMI. Accordingly, adiponectin levels were lower in patients with MetS than in healthy controls (p < 0.05). Leptin, adiponectin, and adipsin did not correlate with the inflammatory cytokine IL-6 or with C-reactive protein (CRP).

Conclusions: The results show that high resistin levels are associated with arthritis independently of MetS, whereas leptin is increased only in arthritis patients with MetS.

Acknowledgements

The excellent technical assistance of Marja-Leena Lampén and Marja Jousimies and the skillful secretarial help of Heli Määttä, the Immunopharmacology Research Group, are acknowledged. We thank Heli Kantola and Tarja Westerlund, Rheumatism Foundation Hospital, for invaluable help. This work was supported by the Research Programme on Nutrition, Foods and Health (ELVIRA) of the National Technology Agency in Finland and by the Competitive Research Funding of the Pirkanmaa Hospital District.

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