Diabetic retinopathy (DR), the most serious diabetic complication, is estimated to account for 4.8% of global blindness [
Omentin-1, a novel visceral fat depot-specific secretary protein, is produced/synthesized by the visceral stromal vascular cells [
To our knowledge, the role of omentin-1 in the pathogenesis of DR has not been examined previously. With this background in mind, we designed this study to investigate the association of serum and vitreous omentin-1 levels with the presence of DR.
A consecutive population of 204 patients who were diagnosed with type 2 diabetes mellitus (T2DM) and underwent vitrectomy were divided into T2DM patients without DR group (
The study was planned according to the ethics guidelines of the Helsinki Declaration and was approved by the Institutional Research Ethics Board of our university. All patients gave written informed consent regarding participation in this study.
Serum was obtained from blood samples by centrifugation and was stored at −80°C until analysis. Vitrectomy samples (approximately 0.3 mL) were got using a standardized vitrectomy technique with manual suction before opening the infusion set. The serum and vitreous samples were analyzed for omentin-1 using commercially available enzyme-linked immunosorbent assay (Cusabio Biotech Corporation, USA).
Data are presented as means ± SD or median (interquartile range). Kolmogorov-Smirnov test was utilized to determine data normality. The differences of characteristics between patients with PDR and NPDR, diabetic patients without DR, and control subjects were compared using Chi-square tests, one-way ANOVA, or Kruskal-Wallis test. Statistical analysis was carried out using SPSS version 13.0 software program (SPSS Inc., Chicago, Illinois).
As shown in Table
Various characteristics of diabetic patients and controls.
Controls | Diabetic patients |
|
|||
---|---|---|---|---|---|
Without DR | NPDR | PDR | |||
|
65 | 60 | 49 | 95 | |
Age (years) | 57.85 ± 6.90 | 58.67 ± 9.00 | 58.16 ± 12.66 | 57.32 ± 10.96 | 0.872 |
Gender (M/F) | 32/33 | 25/35 | 23/26 | 45/50 | 0.852 |
BMI (Kg/m2) | 23.77 ± 1.59 | 23.83 ± 3.00 | 24.32 ± 3.94 | 24.41 ± 3.22 | 0.468 |
SBP (mmHg) | 124.23 ± 11.45 | 141.75 ± 21.74 |
140.51 ± 21.44 |
140.05 ± 23.44 |
<0.001 |
DBP (mmHg) | 83.11 ± 7.63 | 89.25 ± 9.69 |
87.37 ± 13.48 |
87.11 ± 12.20 |
0.016 |
HbA1c (%) | 5.03 ± 0.71 | 7.76 ± 0.95 |
7.82 ± 1.03 |
7.82 ± 1.30 |
<0.001 |
FPG (mmol/L) | 5.11 ± 0.40 | 8.29 ± 1.86 |
8.59 ± 1.50 |
8.10 ± 1.66 |
<0.001 |
TC (mmol/L) | 5.19 ± 0.89 | 5.38 ± 1.40 | 5.33 ± 1.10 | 5.33 ± 1.28 | 0.822 |
TG (mmol/L) | 1.17 ± 0.31 | 1.81 ± 0.58 |
1.85 ± 0.55 |
2.03 ± 0.62 |
0.002 |
LDL-C (mmol/L) | 3.35 ± 0.73 | 3.39 ± 1.06 | 3.36 ± 0.92 | 3.52 ± 1.05 | 0.643 |
HDL-C (mmol/L) | 1.45 ± 0.27 | 1.42 ± 0.40 | 1.43 ± 0.33 | 1.26 ± 0.30 |
0.001 |
Serum and vitreous omentin-1 levels in the four groups are shown in Table
Serum and vitreous omentin-1 levels in controls, diabetic patients without DR, NPDR patients, and PDR patients.
Omentin-1 (ng/mL) | Controls ( |
Without DR ( |
NPDR ( |
PDR ( |
|
---|---|---|---|---|---|
Serum | 208.31 (164.20–251.20) |
184.41 (142.50–206.14) |
166.97 (132.96–199.21) |
139.96 (119.28–157.87) |
<0.001 |
Vitreous | 96.00 (75.24–112.64) |
81.46 (67.84–96.39) |
64.28 (53.08–74.45) |
50.36 (39.91–57.73) |
<0.001 |
Serum/vitreous ratio | 1.99 (1.72–2.63) |
2.17 (1.82–2.57) |
2.72 (2.08–3.37) |
2.88 (2.31–3.48) |
<0.001 |
Serum/vitreous omentin-1 ratio is presented in Table
Omentin-1 is a recently discovered adipokine which is preferentially produced by visceral adipose tissue. Omentin-1 treatment could enhance insulin-stimulated glucose uptake in human adipocytes. In addition, omentin increased Akt phosphorylation in human adipocytes [
Omentin-1 is associated with the presence of diabetic macrovascular complication. Exposure of cardiomyocytes to conditioned media derived from epicardial adipose tissue from patients with T2DM induced contractile dysfunction and insulin resistance, which was prevented by the addition of recombinant omentin [
Omentin-1 is also suggested to be correlated with diabetic microvascular complication. Plasma levels of omentin were found to be markedly higher in end-stage renal disease (ESRD) patients [
Vitreous omentin-1 concentrations are lower than serum omentin-1 concentrations. This indicates that vitreous omentin-1 may be caused by bleeding from the vascular system of the eyes. This hypothesis could explain the similar reduction of plasma and vitreous omentin-1 concentrations. Omentin-1 in eyes may protect the eyes against DR development. And our results showed that serum/vitreous omentin-1 ratio was positively correlated with the presence and severity of DR. This indicates that serum/vitreous omentin-1 ratio may be utilized to predict or assess the development and progression of DR.
Angiogenesis is a key mechanism of DR. Omentin-1 could significantly decrease vascular endothelial growth factor (VEGF) induced endothelial cell migration and angiogenesis in human microvascular endothelial cells [
Omentin-1, one newly discovered adipokine, is shown to be an anti-inflammatory mediator. Omentin was found to inhibit tumor necrosis factor- (TNF-) induced vascular inflammation in human endothelial cells [
In short, serum and vitreous omentin-1 levels, as well as serum/vitreous omentin-1 ratio, are correlated with the presence and severity of DR.
The authors declare that there is no conflict of interests regarding the publication of this paper.