impact factor, citescore
logo
 

Full Papers

 

Implication of CXCL5 (epithelial neutrophil-activating peptide 78) in the development of insulin resistance in patients with rheumatoid arthritis


1, 2, 3, 4, 5, 6

 

  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. Central Laboratory Division, 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, Rheumatology Div., Hosp. Universitario Marqués de Valdecilla, IDIVAL and University of Cantabria, Santander; and Univ. of the Witwatersrand, South Africa.
  6. Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain. iferrazamaro@hotmail.com

CER11239
2019 Vol.37, N°3
PI 0373, PF 0379
Full Papers

Free to view
(click on article PDF icon to read the article)

PMID: 30299246 [PubMed]

Received: 11/03/2018
Accepted : 11/06/2018
In Press: 17/09/2018
Published: 10/05/2019

Abstract

OBJECTIVES:
The chemokine molecule CXCL5 (C-X-C motif chemokine ligand 5, also known as epithelial neutrophil activating peptide 78 -ENA78-) constitutes a link between obesity, inflammation and insulin resistance (IR) in the general population. CXCL5 has also been found to play a role in rheumatoid arthritis (RA) pathogenesis. Since chronic inflammation promotes IR and impairs pancreatic beta cell function in RA patients, we assessed the role of CXCL5 in the development of IR in RA.
METHODS:
Cross-sectional study that encompassed 141 non-diabetic patients with RA. IR assessed by homeostatic model assessment (HOMA2), insulin and C-peptide serum levels and lipid profile, and CXCL5 serum levels were studied. Regression analysis was performed to evaluate how CXCL5 was related to IR, disease activity, and disease characteristics in RA patients.
RESULTS:
HOMA2-IR indexes showed high values for both IR and beta cell production (%B), and low insulin sensitivity (%S) in patients with RA. C reactive protein (beta coef. 0.2 [95%CI -1.5–1.9], p=0.80) and disease activity through DAS28 (beta coef. 13 [95%CI -14–41], p=0.34) revealed no relation with CXCL5. Other disease characteristics, such as disease duration, serological status, or use of methotrexate or anti-TNF alpha therapies, were not associated with CXCL5 serum levels. While glucocorticoids were related to insulin, C-peptide serum levels, and HOMA2-IR and HOMA2-%B-C peptide, the use of prednisone was not associated with CXCL5 serum levels. Insulin and C peptide serum levels and IR indexes showed strong correlations among each other, but not with CXCL5 (insulin r2=-0.034, p=0.69; C peptide r2=-0.050, p=0.56).
CONCLUSIONS:
CXCL5 is not related to IR in RA patients. Therefore, the mechanisms leading to IR in patients with RA may be different from those in the general population.

Rheumatology Article