Reduced Subfatin levels are independently associated with proliferative diabetic retinopathy, unlike Chromogranin-A


AĞBEKTAŞ T., ZONTUL C., Yeter D. Y., TAŞ A., SİLİĞ Y.

Journal of Diabetes and Metabolic Disorders, cilt.25, sa.2, 2026 (ESCI, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 25 Sayı: 2
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1007/s40200-026-01975-8
  • Dergi Adı: Journal of Diabetes and Metabolic Disorders
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, EMBASE, Academic Search Ultimate (EBSCO), Middle East & Africa Database (ProQuest), Health Research Premium Collection (ProQuest)
  • Anahtar Kelimeler: CgA, Diabetes mellitus, Diabetic retinopathy, Glucose, HbA1c, Subfatin
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Purpose: Diabetic retinopathy (DR) is a major microvascular complication of diabetes, characterized by progressive damage to the retinal vasculature. This study aimed to investigate the levels of Subfatin and Chromogranin A (CgA) proteins in patients with DR. Methods: This cross-sectional study included 96 participants divided into three groups: proliferative diabetic retinopathy (PDR), diabetes mellitus without retinopathy (DM), and healthy controls. Serum samples were collected, and Subfatin and CgA protein levels were measured using enzyme-linked immunosorbent assay (ELISA). Results: Glucose levels were significantly higher in both male and female participants in the PDR group than in the DM and control groups (p < 0.05). Serum subfatin levels were lowest in the PDR group compared those to in the DM and control groups, and this difference was statistically significant (p < 0.05). Additionally, a significant correlation was observed between CgA protein levels and weight and BMI, but only in the control group. Conclusions: Subfatin levels were reduced in patients with PDR, accompanied by elevated glucose and HbA1c levels. These findings suggest that reduced subfatin levels may be associated with metabolic and inflammatory alterations involved in the pathophysiology of PDR.