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Serum Adropin Levels in Patients with Rheumatoid Arthritis

Adropin is a secretory protein that mainly modulates metabolic homeostasis and endothelial function. There is growing evidence supporting association of adropin with various inflammatory diseases, including rheumatoid arthritis (RA). This study aimed to compare serum adropin levels between 70 patien...

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Detalles Bibliográficos
Autores principales: Simac, Petra, Perkovic, Dijana, Bozic, Ivona, Bilopavlovic, Nada, Martinovic, Dinko, Bozic, Josko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8875108/
https://www.ncbi.nlm.nih.gov/pubmed/35207457
http://dx.doi.org/10.3390/life12020169
Descripción
Sumario:Adropin is a secretory protein that mainly modulates metabolic homeostasis and endothelial function. There is growing evidence supporting association of adropin with various inflammatory diseases, including rheumatoid arthritis (RA). This study aimed to compare serum adropin levels between 70 patients with RA and 70 matched healthy controls. Furthermore, we explored adropin correlations with RA disease activity, glucose metabolism parameters and inflammatory biomarkers. Serum adropin levels were determined by a competitive enzyme-linked immunosorbent assay. Serum adropin levels were significantly lower in RA patients than in the control group (2.85 ± 0.91 vs. 4.02 ± 0.99 ng/mL, p < 0.001). In the RA group, serum adropin levels had a significant negative correlation with total cholesterol (r = −0.172, p = 0.043), HbA1c (r = −0.406, p < 0.001), fasting glucose (r = −0.377, p < 0.001) and HOMA-IR (the homeostasis model assessment-estimated insulin resistance; (r = −0.315, p = 0.008)). Multiple linear regression analysis showed that serum adropin levels retained a significant association with levels of fasting glucose (β ± SE, −0.450 ± 0.140, p = 0.002) and HbA1c (−0.528 ± 0.223, p = 0.021) after model adjustments. These findings imply that adropin could have an impact on metabolic homeostasis in RA, although further well-designed studies are warranted in order to establish this.