cortistatin-14 and Diabetic-Retinopathy

To evaluate the aqueous humor and serum cortistatin levels in diabetic patients with and without diabetic retinopathy and its relationship with various metabolic markers that have been reported to be associated with diabetes mellitus.. The current study included 20 diabetes mellitus patients with diabetic retinopathy, 20 diabetes mellitus patients without diabetic retinopathy, and 20 healthy control subjects with the same sex and age characteristics. Aqueous humor and serum cortistatin, fasting blood glucose, hemoglobinA1c, 25-hydroxyvitamin D levels, blood lipid profiles, and body mass index were measured in all subjects.. In diabetic patients with and without diabetic retinopathy and in healthy control subjects, the mean aqueous humor cortistatin levels were 25.55 ± 2.03, 27.71 ± 2.01, and 32.76 ± 3.43 ng/mL, respectively. Likewise, the mean serum cortistatin levels were 6.16 ± 1.08, 6.57 ± 1.00, and 7.56 ± 1.51 ng/mL, respectively. Aqueous humor cortistatin levels were decreased in diabetic patients with and without diabetic retinopathy when compared to healthy controls (. Aqueous humor cortistatin levels were decreased in diabetic patients with and without diabetic retinopathy. The results suggest that a local decrease in the amount of cortistatin may play a role in the pathogenesis of diabetic retinopathy.

Topics: Aged; Aqueous Humor; Biomarkers; Diabetes Mellitus; Diabetic Retinopathy; Female; Humans; Male; Middle Aged; Neuropeptides

Cortistatin (CST), a neuropeptide with strong structural and functional similarities to somatostatin, is abundant in the vitreous fluid, and it is decreased in patients with proliferative diabetic retinopathy. The aims of the present study were to explore whether the retina produces CST, and to compare its expression between diabetic and nondiabetic donors. Retinal neurodegeneration was assessed by measuring glial fibrilar acidic protein (GFAP) by confocal laser microscopy and counting the apoptotic TUNEL positive cells in which nuclear fragmentation as well as condensation were present.. Human postmortem eyes (10) from five diabetic donors were compared with 10 eyes from five nondiabetic donors, matched by age. CST mRNA (RT-PCR) and CST (confocal laser microscopy) were measured separately in both the neuroretina and retinal pigment epithelium (RPE). Retinal neurodegeneration was assessed by measuring glial fibrillar acidic protein (GFAP) by confocal laser microscopy and counting the apoptotic cells by TUNEL.. CST was found to be produced by the human retina, and higher levels of CST mRNA were found in RPE than in the neuroretina. CST mRNA levels in diabetic donors were significantly lower in both the RPE (p=0.001) and the neuroretina (p=0.03) in comparison with nondiabetic donors. CST immunofluorescence was in agreement with mRNA expression, but the differences were only significant when comparing neuroretinas (p=0.03). Increased GFAP and a higher degree of apoptosis were observed in diabetic retinas in comparison with nondiabetic retinas. These changes were inversely related with CST levels.. CST is expressed in the human retina. There is more CST in the RPE than in the neuroretina. A lower expression of CST exists in diabetic retinas and it is associated with retinal neurodegeneration.

Topics: Aged; Apoptosis; Case-Control Studies; Diabetic Retinopathy; Female; Glial Fibrillary Acidic Protein; Humans; Male; Middle Aged; Nerve Degeneration; Neuroglia; Neuropeptides; Retina; Tissue Donors

There is growing evidence to indicate that somatostatin could be added to the list of natural antiangiogenic factors that exist in the vitreous fluid. In addition, a deficit of intravitreous somatostatin-like immunoreactivity (SLI) has been found in diabetic patients with proliferative diabetic retinopathy (PDR). In the present study, we have determined the main molecular variants of somatostatin (somatostatin-14 and somatostatin-28) in the vitreous fluid and plasma of nondiabetic control subjects and diabetic patients with PDR. In addition, the contribution of cortistatin, a neuropeptide with strong structural similarities to somatostatin, to SLI and its levels in vitreous and plasma in both nondiabetic and diabetic patients has also been measured. RESERCH DESIGN AND METHODS: Plasma and vitreous fluid from 22 diabetic patients with PDR and 22 nondiabetic control subjects were analyzed. Somatostatin-14, somatostatin-28 and cortistatin were measured by radioimmunoassay but separation by high-performance liquid chromatography was required to measure somatostatin-14.. The predominant molecular form of somatostatin within the vitreous fluid was somatostatin-28 (fivefold higher than somatostatin-14 in control subjects and threefold higher in patients with PDR). Cortistatin significantly contributed to SLI and its intravitreous levels were higher than those detected in plasma (nondiabetic control subjects: 147 [102-837] vs. 78 [24-32] pg/ml; patients with PDR: 187 [87-998] vs. 62 [24-472] pg/ml; P = 0.01 for both). Intravitreous somatostatin-14 was similar in both subjects with PDR and the control group (P = 0.87). By contrast, somatostatin-28 concentration was lower in patients with PDR than in nondiabetic control subjects (350 +/- 32 vs. 595 +/- 66 pg/ml; P = 0.004).. Somatostatin-28 is the main molecular variant in the vitreous fluid. The intravitreous SLI deficit detected in patients with PDR is mainly due to somatostatin-28. Cortistatin is abundant in the vitreous fluid and significantly contributes to SLI. These findings could open up new strategies for PDR treatment.

Topics: Chromatography, High Pressure Liquid; Diabetic Retinopathy; Genetic Variation; Humans; Neuropeptides; Reference Values; Somatostatin; Vitrectomy; Vitreous Body