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Inflammation‐associated insulin resistance: Differential effects in rheumatoid arthritis and systemic lupus erythematosus define potential mechanisms

Inflammation‐associated insulin resistance: Differential effects in rheumatoid arthritis and... Objective Insulin resistance is increased by inflammation, but the mechanisms are unclear. The present study was undertaken to test the hypothesis that decreased insulin sensitivity is differentially associated with mediators of inflammation by studying 2 chronic inflammatory diseases of different pathogenesis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Methods We measured fasting insulin, glucose, and lipid levels, erythrocyte sedimentation rate (ESR), C‐reactive protein (CRP), interleukin‐6 (IL‐6), tumor necrosis factor α (TNFα), and coronary artery calcification in 103 patients with SLE and in 124 patients with RA. Insulin sensitivity was measured using the homeostasis model assessment (HOMA) index. Results The HOMA value was higher in RA patients (median 2.05 (interquartile range (IQR) 1.05–3.54)) than in SLE patients (1.40 (0.78–2.59)) (P = 0.007). CRP and ESR did not differ significantly in RA and SLE patients. Body mass index (BMI) was significantly correlated with the HOMA index in both RA (ρ = 0.20) and SLE (ρ = 0.54), independently of age, sex, race, and current use of corticosteroids. In RA patients, the HOMA index was also significantly positively correlated with IL‐6 (ρ = 0.63), TNFα (ρ = 0.50), CRP (ρ = 0.29), ESR (ρ = 0.26), coronary calcification (ρ = 0.26), and Disease Activity Score in 28 joints (ρ = 0.21); associations adjusted for age, sex, race, BMI, and current use of corticosteroids remained significant (P < 0.05). In SLE patients, the HOMA index was also significantly correlated with ESR (ρ = 0.35) and CRP (ρ = 0.25), but not with other variables. The association between the ESR and the HOMA value in patients with SLE remained significant after adjustment for confounding covariates (P = 0.008). In multivariable models, the major contributing factors to the HOMA index were the BMI in SLE patients, and IL‐6 and TNFα levels in RA patients. Conclusion The pathogenesis of insulin resistance and its contribution to atherogenesis varies in different inflammatory settings. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arthritis & Rheumatism Wiley

Inflammation‐associated insulin resistance: Differential effects in rheumatoid arthritis and systemic lupus erythematosus define potential mechanisms

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References (51)

Publisher
Wiley
Copyright
Copyright © 2008 by the American College of Rheumatology
ISSN
0004-3591
eISSN
1529-0131
DOI
10.1002/art.23600
pmid
18576352
Publisher site
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Abstract

Objective Insulin resistance is increased by inflammation, but the mechanisms are unclear. The present study was undertaken to test the hypothesis that decreased insulin sensitivity is differentially associated with mediators of inflammation by studying 2 chronic inflammatory diseases of different pathogenesis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Methods We measured fasting insulin, glucose, and lipid levels, erythrocyte sedimentation rate (ESR), C‐reactive protein (CRP), interleukin‐6 (IL‐6), tumor necrosis factor α (TNFα), and coronary artery calcification in 103 patients with SLE and in 124 patients with RA. Insulin sensitivity was measured using the homeostasis model assessment (HOMA) index. Results The HOMA value was higher in RA patients (median 2.05 (interquartile range (IQR) 1.05–3.54)) than in SLE patients (1.40 (0.78–2.59)) (P = 0.007). CRP and ESR did not differ significantly in RA and SLE patients. Body mass index (BMI) was significantly correlated with the HOMA index in both RA (ρ = 0.20) and SLE (ρ = 0.54), independently of age, sex, race, and current use of corticosteroids. In RA patients, the HOMA index was also significantly positively correlated with IL‐6 (ρ = 0.63), TNFα (ρ = 0.50), CRP (ρ = 0.29), ESR (ρ = 0.26), coronary calcification (ρ = 0.26), and Disease Activity Score in 28 joints (ρ = 0.21); associations adjusted for age, sex, race, BMI, and current use of corticosteroids remained significant (P < 0.05). In SLE patients, the HOMA index was also significantly correlated with ESR (ρ = 0.35) and CRP (ρ = 0.25), but not with other variables. The association between the ESR and the HOMA value in patients with SLE remained significant after adjustment for confounding covariates (P = 0.008). In multivariable models, the major contributing factors to the HOMA index were the BMI in SLE patients, and IL‐6 and TNFα levels in RA patients. Conclusion The pathogenesis of insulin resistance and its contribution to atherogenesis varies in different inflammatory settings.

Journal

Arthritis & Rheumatism – Wiley

Published: Jul 1, 2008

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