Impaired beta cell function is present in non-diabetic rheumatoid arthritis patients
IntroductionTo investigate how markers of beta cell secretion (proinsulin processing metabolites) are expressed in rheumatoid arthritis (RA) patients and their potential relationship with the insulin resistance (IR) observed in these patients.
101 RA patients and 99 non-diabetic sex- and age-matched controls were included. IR by homeostatic model assessment (HOMA2), and beta cell secretion as measured by insulin, split and intact proinsulin, and C-peptide levels were determined for both groups.
Multiple regression analysis was performed to compare IR between groups and to explore the interrelationships between RA features, proinsulin metabolites, and IR. Data were adjusted for glucocorticoids intake and for IR classical risk factors.
Compared to controls, RA patients showed higher HOMA-IR (beta coef ., 0.40 [95%CI 0.20-0.59], p=0.00).
When data were adjusted for glucocorticoids intake, non-corticosteroid patients maintained a higher IR index (beta 0.14 [0.05-0.24], p=0.00). Impaired insulin processing in RA patients was detected by the onset of elevated split proinsulin levels (beta 0.70 p/molL [0.38-1.02], p=0.00).
This data remained also significant when adjusted for prednisone intake (beta 0.19 [0.00-0.36], p=0.04). Split proinsulin to C-peptide ratios were higher in RA patients undergoing corticosteroid therapy (beta 0.25 pmol/L [0.12-0.38] p=0.03) and were nearly significant in comparison between non-corticosteroids patients and controls (beta 0.16 pmol/L [-0.02-0.34], p=0.08).
Interestingly, the impact of HOMA-IR on the ratio of intact proinsulin to C-peptide was higher in controls compared to patients (beta 6.23 [1.41-11.06] vs. 0.43 [-0.86-1.71], p=0.03).
Beta cell function is impaired in non-diabetic and non-on corticoids RA patients by a mechanism that seems to be, at least in part, independent of IR.
Published on: 2013-01-22