title: Somatostatin molecular variants in the vitreous fluid: a comparative study between diabetic patients with proliferative diabetic retinopathy and nondiabetic control subjects.
abstract: 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. 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.
  
  
  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.
authors.affiliation: Diabetes Research Unit, Endocrinology Division, Hospital Universitari Vall d'Hebron, Pg. Vall d'Hebron 119-129, 08035 Barcelona, Spain.
authors.forename: Cristina
authors.initials: C
authors.lastname: Hernández
authors.forename: Esther
authors.initials: E
authors.lastname: Carrasco
authors.forename: Roser
authors.initials: R
authors.lastname: Casamitjana
authors.forename: Ramon
authors.initials: R
authors.lastname: Deulofeu
authors.forename: José
authors.initials: J
authors.lastname: García-Arumí
authors.forename: Rafael
authors.initials: R
authors.lastname: Simó
mesh_terms: D002851:Chromatography, High Pressure Liquid; D003930:Diabetic Retinopathy / Q000235:genetics*; D014644:Genetic Variation; D006801:Humans; D009479:Neuropeptides / Q000032:analysis; D012016:Reference Values; D013004:Somatostatin / Q000235:genetics*; D014821:Vitrectomy; D014822:Vitreous Body / Q000737:chemistry* / Q000502:physiology / Q000503:physiopathology
chemical_list: D009479:Neuropeptides; C099323:cortistatin; D013004:Somatostatin