Somatostatin molecular variants in the vitreous fluid: A comparative study between diabetic patients with proliferative diabetic retinopathy and nondiabetic control subjects
Diabetes Care, ISSN: 0149-5992, Vol: 28, Issue: 8, Page: 1941-1947
2005
- 63Citations
- 35Captures
- 1Mentions
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Metrics Details
- Citations63
- Citation Indexes63
- 63
- CrossRef47
- Captures35
- Readers35
- 32
- Mentions1
- References1
- Wikipedia1
Article Description
OBJECTIVE - 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. RESEARCH 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. RESULTS - 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). CONCLUSIONS - 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. © 2005 by the American Diabetes Association.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=23044508458&origin=inward; http://dx.doi.org/10.2337/diacare.28.8.1941; http://www.ncbi.nlm.nih.gov/pubmed/16043736; https://diabetesjournals.org/care/article/28/8/1941/23816/Somatostatin-Molecular-Variants-in-the-Vitreous; https://dx.doi.org/10.2337/diacare.28.8.1941; https://care.diabetesjournals.org/content/28/8/1941
American Diabetes Association
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