Plasma pentraxin-3 is associated with endothelial dysfunction in non-alcoholic fatty liver disease
European review for medical and pharmacological sciences, cilt.20, sa.20, ss.4305-4312, 2016 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 20 Sayı: 20
- Basım Tarihi: 2016
- Dergi Adı: European review for medical and pharmacological sciences
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.4305-4312
- Anahtar Kelimeler: Pentraxin-3, Endothelial dysfunction, Non-alcoholic fatty liver disease
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
OBJECTIVE: Pentraxin-3 (PTX-3) is an acute-phase protein belonging to the PTX family. It has been reported that PTX-3 is significantly associated with obesity, metabolic syndrome, and cardiovascular diseases (CVD). Non-alcoholic fatty liver disease (NAFLD) is strongly associated with atherosclerosis and CVD. In this study, we aimed to investigate the relationship of PTX-3 with circulating markers of endothelial dysfunction and atherosclerosis in patients with NAFLD. PATIENTS AND METHODS: Seventy patients with biopsy-proven NAFLD and seventy healthy controls were enrolled in the study. Plasma asymmetric dimethylarginine (ADMA), adiponectin, and PTX-3 levels were determined using enzyme-linked immunosorbent assay (ELISA). High-sensitivity C-reactive protein (hsCRP) serum levels were measured with the immunoturbidimetric assay. Insulin resistance was estimated using the HOMA-IR index. RESULTS: PTX-3 and hsCRP levels were higher and adiponectin levels were lower in the NAFLD group compared to the healthy controls (p < 0.001 for all). In correlation analysis, a significant association was observed between PTX-3 and ADMA levels (r = 0.423, p < 0.001). CONCLUSIONS: Our study demonstrated for the first time that increased circulating PTX-3 is strongly associated with endothelial dysfunction in subjects with NAFLD. However, large prospective studies are needed to establish the independent predictive value of PTX-3 for CVD endpoints in this clinically relevant condition.