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Objectives It has been suggested that resistance to insulin action is a feature that accompanies rheumatoid arthritis (RA), a disease where chronic inflammation predominates and classical triggers for insulin resistance (IR) like obesity and diabetes are absents. However, data regarding characterization of RA features associated with this insulin resistance (IR) are lacking. The aim of this study was to investigate how sensitivity to insulin and markers of beta cell dysfunction (proinsulin processing metabolites) are expressed in RA. Methods 101 non-diabetic RA patients and 99 non-diabetic sex and age-matched controls were included in this study. Insulin sensitivity function through homeostatic model assessment (HOMA2), and beta cell secretion through insulin, split and intact proinsulin, and C-peptide were assessed in both groups. We performed multiple regression analysis to compare IR between groups and to explore the relation between RA features and IR. Data were adjusted for glucocorticoids intake and for IR classical risk factors. Results RA patients compared to controls show higher HOMA-IR ( log HOMA-IR, beta coefficient, 0.40 [95% CI 0.20-0.59], p=0.00). When this data was adjusted for glucocorticoids intake, non-on corticosteroid patients maintained a higher IR index (beta coef. 0.14 [95% CI 0.05-0.24], p=0.00). Current prednisone treatment was not associated with higher IR in the patients’ intragroup comparison (beta coef. 0.56 [1.13-1.19], p=0.22). Insulin processing signaling in RA patients showed impaired features via an elevated intact proinsulin levels (beta coef. 3.13 [0.81-5.44] pMol/L, p=0.03 for the comparison between patients and controls). Split proinsulin levels were also higher in RA patients (beta coef. 13.7 pmol/L [3.57-9.40], p=0.00) even adjusting for prednisone intake (beta coef. 2.66 pmol/L [95%CI 1.62-5.95] for non steroids RA patients when compared to controls). In multiple regression analysis, RA features (disease duration, rheumatoid factor, erythrocyte sedimentation rate, C-reactive protein, disease activity through HAQ and DAS28 scores, and current non-biologic disease modifying antirheumatic drug), when adjusted for sex, age and body mass index, were not associated with IR or insulin propeptides. Conclusions Beta cell signaling is impaired in non-diabetic and non-corticoids RA patients. Disclosure of Interest None Declared

Objectives The retinol binding protein 4 (RBP4) has recently been described as a protein highly related with insulin resistance (IR) states like obesity and diabetes. The chronic inflammatory states, like in rheumatoid arthritis (RA), are linked also to insulin resistance by mechanisms that are unknown. Therefore, RA is considered as an insulin resistance model related with a chronic inflammatory state, where diabetes and obesity, classical factors for IR, are absent. The objective of this study is to estimate RBP4 expression in RA patients. Methods 101 RA patients and 115 age and sex-matched controls were included. Pancreatic beta cell function was estimated by classical insulinresistance indexes like HOMA (homeostatic model assessment 2). RBP4, C peptide and insuline levels were measured in patients and controls by a specific enzyme-linked immunosorbent assay (ELISA). Multivariate analysis was performed to compare results between patients and controls and the data were adjusted for glucocorticoids intake and for IR classical risk factors. Results RBP4 levels did not show differences between controls and patients, after adjusting for sex, age, body mass index (BMI) and waist circumference (lnRBP4 2,83 mcg/dl in patients vs. 2,70 mcg/dl, p=0,33). On going steroids patients showed higher RBP4 levels (lnRBP4 3,03 vs 2,61 mcg/dl, p=0.00), after adjusting for age, sex, BMI and waist circumference. Similarly, in the univariate analysis, RBP4 levels tended to correlate with steroid average dose (r=0,20, p=0,14). In our serie, RBP4 levels were not related with the classical IR characteristics, like abdominal waist and BMI, both in controls and patients. Nor these levels showed relation with ESR, CRP, insuline levels or disease activity indexes. Conclusions The molecular mechanisms that lead to IR in RA patients appear to be different from those that ocurr in obesity and diabetes status. RBP4 does not seem to play a role in IR in patients with RA. Disclosure of Interest None Declared