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Amylin in the insulin resistance of patients with rheumatoid arthritis

1, 2, 3, 4, 5, 6, 7, 8

 

  1. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
  2. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain.
  3. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
  4. Central Laboratory Division, Hospital Universitario de Canarias, Tenerife, Spain.
  5. Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain.
  6. Division of Internal Medicine, Hospital Universitario Marqués de Valdecilla, IDIVAL, Universidad de Cantabria, RETICEF, Santander, Spain.
  7. Division of Internal Medicine, Hospital Universitario Marqués de Valdecilla, IDIVAL, Universidad de Cantabria, RETICEF, Santander, Spain.
  8. Epidemiology, Genetics & Atherosclerosis Res. Group on Systemic Inflammatory Diseases, and Div.of Rheumatology, Hosp.Univ. Marqués de Valdecilla, IDIVAL, University of Cantabria, Santander, Spain; and Univ. of the Witwatersrand, Johannesburg, South Africa

CER10679
2018 Vol.36, N°3
PI 0421, PF 0427
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PMID: 29352842 [PubMed]

Received: 11/07/2017
Accepted : 11/09/2017
In Press: 15/01/2018
Published: 17/05/2018

Abstract

OBJECTIVES:
Amylin, which is co-secreted with insulin, plays a role in glycemic regulation and is impaired in type 2 diabetes. In the present study we assess, for the first time, the implication of amylin in the development of insulin resistance (IR) in rheumatoid arthritis (RA).
METHODS:
This was a cross-sectional study involving 361 non-diabetic individuals, 151 patients with RA and 210 sex-matched controls. Insulin, C-peptide, amylin, lipoprotein serum concentrations, and IR indexes by homeostatic model assessment (HOMA2) were evaluated in patients and controls. A multivariable analysis, adjusted for IR-related factors, was performed to determine the differences between patients and controls vis-à-vis amylin and how it is related to IR in RA.
RESULTS:
Insulin, C-peptide and HOMA2-IR indexes were higher in RA patients than in controls. Amylin serum levels were found to be upregulated in RA patients compared to controls (1.36 ± 0.81 vs. 1.79 ± 1.51 ng/ml, p=0.011), although this difference was lost after adjusting for covariates (p=0.46). While amylin positively correlated with the presence of rheumatoid factor (beta coef. 0.90 [95%CI -0.23–1.56], p=0.009) and SDAI (beta coef 0.01 [95%CI 0.00–0.03], p=0.034), no significant association with other disease activity scores, glucocorticoid intake, methotrexate use or TNF-alpha inhibitors was found.
CONCLUSIONS:
IR in RA does not appear to be mediated by amylin. This would imply that the mechanisms associated with IR in RA patients differ from those at work in type 2 diabetes.

Rheumatology Article