title: Analysis of G(-174)C IL-6 polymorphism and plasma concentrations of inflammatory markers in patients with type 2 diabetes and peripheral arterial disease.
abstract: OBJECTIVE
  To determine whether the G(-174)C interleukin 6 (IL-6) polymorphism influences the development of peripheral arterial disease (PAD) in individuals with type 2 diabetes. This was investigated by comparing the distribution of G(-174)C genotypes between patients with type 2 diabetes and PAD (PAD+) and those with type 2 diabetes but without PAD (PAD-). Plasma concentrations of IL-6, fibrinogen, C reactive protein (CRP), and vascular endothelial growth factor (VEGF) were also compared in PAD+ and PAD- patients.
  
  
  METHODS
  Blood samples were collected from 146 PAD+ and 144 PAD- patients. SfaNI was used to determine the G(-174)C genotype. Plasma concentrations of IL-6, fibrinogen, CRP, and VEGF were measured by an enzyme linked immunosorbent assay.
  
  
  RESULTS
  The GG genotype was more common in PAD+ patients than in PAD- patients. PAD+ patients also had increased mean plasma concentrations of IL-6, fibrinogen, CRP, and VEGF compared with PAD- patients. Mean plasma concentrations of IL-6, fibrinogen, and CRP in both PAD+ and PAD- patients were higher in those with the GG genotype than in those with the GC or CC genotypes. In contrast, mean plasma concentrations of VEGF in PAD+ and PAD- patients were not significantly different between those with different G(-174)C genotypes.
  
  
  CONCLUSIONS
  These results support a model in which the GG genotype promotes PAD development among individuals with type 2 diabetes by inducing increased release of IL-6. Higher concentrations of IL-6 among those with the GG genotype is associated with increased plasma concentrations of fibrinogen and CRP.
authors.affiliation: Department of Biomedical Sciences, University of Catania, Via Androne, 83-95124, Catania, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Libra
authors.forename: S S
authors.initials: SS
authors.lastname: Signorelli
authors.forename: Y
authors.initials: Y
authors.lastname: Bevelacqua
authors.forename: P M
authors.initials: PM
authors.lastname: Navolanic
authors.forename: V
authors.initials: V
authors.lastname: Bevelacqua
authors.forename: J
authors.initials: J
authors.lastname: Polesel
authors.forename: R
authors.initials: R
authors.lastname: Talamini
authors.forename: F
authors.initials: F
authors.lastname: Stivala
authors.forename: M C
authors.initials: MC
authors.lastname: Mazzarino
authors.forename: G
authors.initials: G
authors.lastname: Malaponte
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D003925:Diabetic Angiopathies / Q000097:blood / Q000235:genetics*; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D015850:Interleukin-6; D042461:Vascular Endothelial Growth Factor A; D005340:Fibrinogen; D002097:C-Reactive Protein