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Comparative Study
Retinol-binding protein 4 in rheumatoid arthritis-related insulin resistance and β-cell function.
- Iván Ferraz-Amaro, Miguel A González-Gay, and Federico Diaz-González.
- From the Rheumatology Division, Hospital Universitario de Canarias, Tenerife; Rheumatology Division, Hospital Universitario Marqués de Valdecilla, IFIMAV, Santander; Departamento de Medicina, Facultad de Medicina, Universidad de La Laguna, Tenerife, Spain.
- J Rheumatol. 2014 Apr 1; 41 (4): 658-65.
ObjectiveRetinol-binding protein 4 (RBP4), an adipokine related to impaired glucose tolerance, has been associated with insulin resistance (IR) and β-cell function in subjects with obesity or diabetes. In our study we assessed RBP4 levels in patients with rheumatoid arthritis (RA). We also determined whether any correlation exists between RBP4 levels and the presence of IR in these patients.MethodsPlasma RBP4, insulin, C-peptide concentrations, and homeostasis model assessment (HOMA)-IR were measured in 101 patients with RA and 115 sex-matched and age-matched controls. A multivariable analysis adjusted for IR classic cardiovascular risk factors and body mass index was performed to establish the correlation between RBP4 plasma concentrations and features of IR in RA. Data were adjusted for glucocorticoid intake in patients with RA.ResultsPatients had higher levels of insulin, C-peptide levels, HOMA-percentage of β-cell secretion (%B) index, and HOMA-IR index than controls. RBP4 levels were significantly lower in the whole group of patients than in controls [13.99 (9.78-19.88) vs 21.50 (10.28-32.59) μg/ml, p<0.01]. However, only those who were glucocorticoid-naive showed significant difference in RBP4 plasma concentration when compared to controls [11.88 (7.93-17.96) vs 21.50 (10.28-32.59) μg/ml, p<0.01]. The HOMA-%B [log β coefficient 0.00 (0.00-0.01), p<0.01] showed positive relationships regarding RBP4 in controls. That was not the case in patients with RA [log β coefficient 0.00 (-0.0-0.00), p=0.93 for HOMA-%B].ConclusionRBP4 does not correlate with the presence of IR and β-cell function in patients with RA. The mechanisms leading to IR in RA may be different from those occurring in obesity or diabetes.
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