A recent study published in Medicine (Baltimore)reported higher serum asprosin levels in patients with rheumatoid arthritis (RA) than in healthy controls. However, the difference was no longer statistically significant after adjustment for potential confounders. The findings suggest that although asprosin may be involved in inflammatory pathways, its clinical utility as an independent biomarker in RA remains uncertain.
Adipokines have gained increasing attention in RA research because of their involvement in metabolic regulation and immune-mediated inflammation. Several adipokines, including leptin, visfatin, adiponectin, and resistin, have been implicated in synovial inflammation and joint damage. Asprosin, a recently identified glucogenic adipokine secreted by white adipose tissue during fasting, primarily regulates glucose homeostasis. Emerging experimental evidence also suggests that it may contribute to inflammatory processes by promoting proinflammatory cytokine production.
The single-centre, cross-sectional observational study included 42 patients with RA and 40 controls recruited between June and August 2025. Serum asprosin concentrations were measured using enzyme-linked immunosorbent assay (ELISA), while RA disease activity was evaluated using the Disease Activity Score in 28 joints based on erythrocyte sedimentation rate (DAS28-ESR).
Median (interquartile range) serum asprosin levels were significantly higher in patients with RA than in controls (12.43 [9.98] vs 9.96 [3.47] ng/mL; P = .025). However, the association was no longer statistically significant after adjustment for age, sex, body mass index, smoking status, and comorbidities (adjusted P = .986). Furthermore, asprosin levels showed no significant correlations with DAS28-ESR, C-reactive protein, erythrocyte sedimentation rate, rheumatoid factor, or anti-cyclic citrullinated peptide antibodies. Receiver operating characteristic analysis demonstrated modest discriminatory ability, with an area under the curve of 0.643 (95% CI, 0.52–0.767; P = .02).
These findings differ from those of an earlier case-control study by Xu et al., which included 205 patients with RA and 205 healthy controls. That study reported significantly elevated plasma asprosin concentrations in patients with RA (11.4 [8.2–15.6] vs 9.3 [7.5–10.5] ng/mL; P < .001), with an area under the curve of 0.67. Experimental investigations using MH7A synovial fibroblasts further demonstrated that asprosin enhanced cellular proliferation, proinflammatory cytokine expression, migration, and invasion, suggesting a possible contribution to RA-associated synovial pathology. Tumour necrosis factor-α-mediated downregulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) was associated with increased asprosin levels, whereas treatment with rosiglitazone attenuated asprosin overproduction.
These studies highlight a potential link between asprosin and RA pathophysiology, while underscoring the distinction between experimental evidence of inflammatory activity and clinical biomarker performance. Although elevated circulating asprosin levels have been observed in RA, the absence of an independent association after adjustment for confounders, along with its lack of correlation with established disease activity measures, limits its current relevance as a standalone biomarker. Larger prospective studies are warranted to determine whether asprosin contributes to RA pathogenesis and whether it offers additional clinical value beyond conventional inflammatory and serological markers.
References
- Zontul S, Kaya Z, Aydoğdu MS, İnanç E, Çetin M, Yolbaş S, Arslan AK, Uçar C. Serum asprosin levels in patients with rheumatoid arthritis: An exploratory cross-sectional study. Medicine (Baltimore). 2026 Sep 25;105(39):e50802.
- Xu SZ, Tao SS, Wang P, Wei HF, Tan YT, Tang J, Chen Z, Pan HF. Elevated asprosin expression exacerbates synovial inflammation by PPAR-γ-dependent mechanisms in rheumatoid arthritis. Clin Immunol. 2026 Apr;284:110677.