Resistencia insulínica y artritis reumatoide

Ferraz-Amaro, Iván; González, Federico Díaz; Juanatey, Carlos González

doi:10.1016/j.reuma.2010.03.010

Cited by 11 publications

(6 citation statements)

References 31 publications

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“…For the purpose of inclusion in the present study, RA disease duration was required to be ≥ 1 year. Although anti-TNF-α treatment has been associated with changes in IR [ 5 , 13 – 15 ], patients with RA undergoing TNF-α antagonist therapy were not excluded in the present study. The control group consisted of patients recruited from the Spanish Camargo Cohort [ 16 , 17 ].…”

Section: Methodsmentioning

confidence: 99%

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Incretins in patients with rheumatoid arthritis

et al. 2017

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BackgroundThe precise mechanism linking systemic inflammation with insulin resistance (IR) in rheumatoid arthritis (RA) remains elusive. In the present study, we determined whether the incretin-insulin axis and incretin effect are disrupted in patients with RA and if they are related to the IR found in these patients.MethodsWe conducted a cross-sectional study that encompassed 361 subjects without diabetes, 151 patients with RA, and 210 sex-matched control subjects. Insulin, C-peptide, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP), dipeptidyl peptidase 4 (DPP-4) soluble form, and IR indexes by homeostatic model assessment (HOMA2) were assessed. A multivariable analysis adjusted for IR-related factors was performed. Additionally, ten patients and ten control subjects underwent a 566-kcal meal test so that we could further study the postprandial differences of these molecules between patients and control subjects.ResultsInsulin, C-peptide, and HOMA2-IR indexes were higher in patients than in control subjects. This was also the case for GLP-1 (0.49 ± 1.28 vs. 0.71 ± 0.22 ng/ml, p = 0.000) and GIP (0.37 ± 0.40 vs. 1.78 ± 0.51 ng/ml, p = 0.000). These differences remained significant after multivariable adjustment including glucocorticoid intake. Disease Activity Score in 28 joints with erythrocyte sedimentation rate (β coefficient 46, 95% CI 6–87, p = 0.026) and Clinical Disease Activity Index (β coefficient 7.74, 95% CI 1.29–14.20, p = 0.019) were associated with DPP-4 serum levels. GLP-1 positively correlated with β-cell function (HOMA2 of β-cell production calculated with C-peptide) in patients but not in control subjects (interaction p = 0.003). The meal test in patients with RA revealed a higher total and late response AUC for glucose response, a later maximal response of C-peptide, and a flatter curve in GIP response.ConclusionsThe incretin-insulin axis, both during fasting and postprandial, is impaired in patients with RA.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-017-1431-9) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

“…Several studies have shown an increased prevalence of IR in patients with rheumatoid arthritis (RA) [ 5 – 7 ], a finding potentially associated with the degree of RA disease activity [ 8 ]. It is thought that low-grade inflammation may contribute to its development [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Incretins in patients with rheumatoid arthritis

et al. 2017

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“…Insulin resistance is an essential feature of MS that has been linked to RA [43]. In a study that included 94 patients with RA, Dessein and Joffe [44] observed that insulin resistance was associated with markers for inflammation such as C-reactive protein and erythrocyte sedimentation rate and disease activity scores.…”

Section: Insulin Resistance and Rheumatoid Arthritismentioning

confidence: 99%

Metabolic Syndrome in Rheumatoid Arthritis

Ferraz-Amaro

González‐Juanatey

López‐Mejías

et al. 2013

Mediators of Inflammation

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Insulin resistance is an essential feature of the metabolic syndrome that has been linked to rheumatoid arthritis (RA). Understanding how inflammation arising in one tissue affects the physiology and pathology of other organs remains an unanswered question with therapeutic implications for chronic conditions including obesity, diabetes mellitus, atherosclerosis, and RA. Adipokines may play a role in the development of atherogenesis in patients with RA. Biologic therapies, such as TNF-α antagonists, that block proinflammatory cytokines have beneficial effects on the insulin resistance that is often observed in patients with RA.

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“…Several reports have linked clinical RA activity with a reduction in peripheral insulin sensitivity [3-7]. Insulin resistance (IR) refers to a state in which a given concentration of insulin is associated with a subnormal glucose response [8].…”

Section: Introductionmentioning

confidence: 99%

Impaired beta cell function is present in nondiabetic rheumatoid arthritis patients

et al. 2013

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IntroductionTo investigate how markers of β-cell secretion (proinsulin-processing metabolites) are expressed in rheumatoid arthritis (RA) patients and their potential relation with the insulin resistance (IR) observed in these patients.MethodsThe 101 RA patients and 99 nondiabetic sex- and age-matched controls were included. IR by homeostatic model assessment (HOMA2), and β-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 interrelations between RA features, proinsulin metabolites, and IR. Data were adjusted for glucocorticoids intake and for IR classic risk factors.ResultsCompared with controls, RA patients showed higher HOMA-IR (β coef., 0.40 (95% CI, 0.20 to 0.59); P = 0.00). When data were adjusted for glucocorticoids intake, noncorticosteroid patients maintained a higher IR index (β, 0.14 (0.05 to 0.24); P = 0.00). Impaired insulin processing in RA patients was detected by the onset of elevated split proinsulin levels (β, 0.70 pmol/L (0.38 to 1.02); P = 0.00). These data remained significant also when adjusted for prednisone intake (β, 0.19 (0.00 to 0.36) pmol/L; P = 0.04). Split proinsulin-to-C-peptide ratios were higher in RA patients undergoing corticosteroid therapy (β, 0.25 (0.12 to 0.38); P = 0.03) and were nearly significant in comparison between noncorticosteroids patients and controls (β, 0.16 (-0.02 to 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 with patients (β, 6.23 (1.41 to 11.06) versus 0.43 (-0.86 to 1.71); P = 0.03).Conclusionsβ-Cell function is impaired in nondiabetic and in RA patients not taking corticoids by a mechanism that seems to be, at least in part, independent of IR.

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Resistencia insulínica y artritis reumatoide

Cited by 11 publications

References 31 publications

Incretins in patients with rheumatoid arthritis

Incretins in patients with rheumatoid arthritis

Metabolic Syndrome in Rheumatoid Arthritis

Impaired beta cell function is present in nondiabetic rheumatoid arthritis patients

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