Arthritis & Rheumatism, Volume 63,
November 2011 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Chicago, Illinois November 4-9, 2011.

Inflammation-Dependent Insulin Resistance Is Present in Rheumatoid Arthritis but it Is Not Associated with Retinol Binding Protein 4.

Hernandez-Hernandez1,  Vanesa, Delgado-Frias1,  Esmeralda, Ferraz-Amaro1,  Ivan, Garcia-Dopico2,  Jose A., Medina2,  Lilian, Gonzalez-Diaz3,  Antonieta, Gomez-Rodriguez-Bethencourt3,  Maria A.

Rheumatology Service, La Laguna, Spain
Laboratorio Central, La Laguna, Spain
Medicina Nuclear, Spain
Resonancia Magnetica IMETISA
Hospital Universitario de Canarias, La Laguna, Spain


Insulin resistance has been associated with rheumatoid arthritis (RA) disease activity. These correlation suggests that inflammation and hyperinsulinemia somehow interact and facilitate one another. Mechanistic data for inflammation-associated insulin resistance in RA are sparse. Retinol binding protein 4 (RBP4), an adipokie that contributes to insulin resistance, is increased in insulin-resistant states like diabetes and obesity. The role of this RBP4 has not been explored in inflammation-associated insulin resistance of RA patients. The purpose of this study was to estimate beta cell function, and resistance and sensitivity to insulin in patients with AR compared to controls, and to describe the potential relationship between peripheral bloods levels of RBP4 and inflammation-associated insulin resistance in RA patients.


216 subjects, 101 RA patients and 115 age and sex matched controls were included in this cross-sectional study. Demographic data regard body mass index, presence of hypertension and corticosteroids intake were collected. Diabetes patients or controls were excluded. We measured in both groups fasting insulin and C-peptide, glucose, lipid levels, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), retinol binding protein 4, interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFalpha). Insulin sensitivity was measured using the homeostasis model assessment index (updated HOMA model 2) to estimate beta cell function (%B), insulin sensitivity (%S) and insulin resistance index (IR). The Health Assessment Questionnaire Disability Index (HAQ) and the Disease Activity Score (DAS 28) were determined in RA patients.


RA patients included were 55.2±10.0 years old, had a mean disease duration of 7.4±5.8 years and show a DAS28 3.99±1.41 and HAQ 0.80±0.76. In the univariate analyses the presence of RA was associated with a higher IR (b coefficient 0.8, 0.2–1.4 IC95%, p=0.01), and %B (b 20%, 2–39 IC95%, p=0,03). Insulinemia was also higher in AR patients, 73.3 vs 95.9 pmol/L, p=0,04 but they did not express higher levels of RBP4. This data remained statiscally significant when adjusted for body mass index, age, presence of comorbility and corticoids intake. DAS28 and HAQ did not correlate with insulin resistance indexes neither RBP4 levels. Similarly, ESR, RCP, IL6 and TNFalpha levels in RA patients were not associated with insulin resistance except for a strong positive association between RCP and %S (r2=0.48, p=0.00). Multivariate analysis was perform to assess whether AR specific factors like ESR, RCP, corticoids intake, DAS28, HAQ, disease duration, and TNFalpha and IL6 levels were able to predict insulin sensitivity, resistance or beta cell function. DAS28, HAQ, corticoids, IL6, TNFa were capable to explain nearly the 20% of IR. For beta cell production, disease duration, corticoids, CRP and TNFalpha, IL6 levels predict 32% of %B variability.


Our data suggest that inflammation and IR interact and facilitate one another. IR states are presence in RA. RBP4 does not seem to play a role in IR related to RA.

To cite this abstract, please use the following information:
Hernandez-Hernandez, Vanesa, Delgado-Frias, Esmeralda, Ferraz-Amaro, Ivan, Garcia-Dopico, Jose A., Medina, Lilian, Gonzalez-Diaz, Antonieta, et al; Inflammation-Dependent Insulin Resistance Is Present in Rheumatoid Arthritis but it Is Not Associated with Retinol Binding Protein 4. [abstract]. Arthritis Rheum 2011;63 Suppl 10 :1166

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