Serum Visfatin and Fetuin-A Levels and Glycemic Control in Patients with Obese Type 2 Diabetes Mellitus
Background: Visfatin is an adipokine produced by visceral adipose tissue and has insulin-mimicking effects. Fetuin-A is a he-patic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. The authors of the present study aimed to investigate the levels...
Gespeichert in:
Veröffentlicht in: | Diabetes & metabolism journal 2011-10, Vol.35 (5), p.523 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | kor |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Background: Visfatin is an adipokine produced by visceral adipose tissue and has insulin-mimicking effects. Fetuin-A is a he-patic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. The authors of the present study aimed to investigate the levels of serum visfatin and fetuin-A and their correlation with hemoglobin A1c (HbA1c) and urine albumin levels in patients with type 2 diabetes mellitus (T2DM). Methods: A total of 40 obese patients with T2DM (11 males and 29 females; age, 54.47±10.83 years and 23 obese nondiabetic controls (8 males and 15 females; age, 53.04±11.33 years) were included in the study. Age, sex, and body mass index were similar in the 2 groups. Serum visfatin and fetuin-A levels were measured by enzyme-linked immunosorbent assay. HbA1c and urine al-bumin levels were measured by high performance liquid chromatography and nephelometric method, respectively. Results: Serum levels of visfatin in patients with T2DM (4.03±2.44 ng/mL) were similar to the control group (3.65±3.02 ng/mL). Serum fetuin-A levels were significantly lower in patients with T2DM than the controls (298.75±78.86 and 430.73±94.46 μg/mL, respectively). HbA1c levels were significantly higher in the T2DM group compared with controls (7.33±1.32 and 5.44±0.84%, respectively). Correlations between visfatin, fetuin-A and HbA1c levels were not observed. Conclusion: The present study suggests fetuin-A may play a role in the pathogenesis of T2DM. |
---|---|
ISSN: | 2233-6079 |