title: Impact of type 2 diabetes on the plasma levels of vascular endothelial growth factor and its soluble receptors type 1 and type 2 in patients with peripheral arterial disease.
abstract: OBJECTIVE
  Type 2 diabetes coexistent with lower extremity artery disease (peripheral arterial disease (PAD)) can be observed in numerous patients. The mechanism compensating for ischemia and contributing to healing is angiogenesis-the process of forming new blood vessels. The purpose of this study was to assess the likely impact of type 2 diabetes on the plasma levels of proangiogenic factor (vascular endothelial growth factor A (VEGF-A)) and angiogenesis inhibitors (soluble VEGF receptors type 1 and type 2 (sVEGFR-1 and sVEGFR-2)) in patients with PAD.
  
  
  METHODS
  Among 46 patients with PAD under pharmacological therapy (non-invasive), we identified, based on medical history, a subgroup with coexistent type 2 diabetes (PAD-DM2+, n=15) and without diabetes (PAD-DM2-, n=31). The control group consisted of 30 healthy subjects. Plasma levels of VEGF-A, sVEGFR-1, and sVEGFR-2 were measured using the enzyme-linked immunosorbent assay (ELISA) method.
  
  
  RESULTS
  The subgroups of PAD-DM2+ and PAD-DM2- revealed significantly higher concentrations of VEGF-A (P=0.000 007 and P=0.000 000 1, respectively) and significantly lower sVEGFR-2 levels (P=0.02 and P=0.000 01, respectively), when compared with the control group. Patients with PAD and coexistent diabetes tended to have a lower level of VEGF-A and higher levels of sVEGFR-1 and sVEGFR-2 comparable with non-diabetic patients.
  
  
  CONCLUSIONS
  The coexistence of type 2 diabetes and PAD is demonstrated by a tendency to a lower plasma level of proangiogenic factor (VEGF-A) and higher levels of angiogenesis inhibitors (sVEGFR-1 and sVEGFR-2) at the same time. Regardless of the coexistence of type 2 diabetes, hypoxia appears to be a crucial factor stimulating the processes of angiogenesis in PAD patients comparable with healthy individuals, whereas hyperglycemia may have a negative impact on angiogenesis in lower limbs.
authors.affiliation: Department of Pathophysiology, Faculty of Pharmacy, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-094, Poland.|Clinic of Vascular and Internal Medicine, Dr. Jan Biziel University Hospital No. 2 in Bydgoszcz, Bydgoszcz PL 85-168, Poland.
authors.forename: Radosław
authors.initials: R
authors.lastname: Wieczór
authors.affiliation: Department of Pathophysiology, Faculty of Pharmacy, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-094, Poland.
authors.forename: Grażyna
authors.initials: G
authors.lastname: Gadomska
authors.affiliation: Department of Pathophysiology, Faculty of Pharmacy, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-094, Poland.
authors.forename: Barbara
authors.initials: B
authors.lastname: Ruszkowska-Ciastek
authors.affiliation: Department of Pathophysiology, Faculty of Pharmacy, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-094, Poland.
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Stankowska
authors.affiliation: Clinic of Vascular and Internal Medicine, Dr. Jan Biziel University Hospital No. 2 in Bydgoszcz, Bydgoszcz PL 85-168, Poland.|Department of Vascular and Internal Medicine, Faculty of Health Sciences, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-168, Poland.
authors.forename: Jacek
authors.initials: J
authors.lastname: Budzyński
authors.affiliation: Clinic of Vascular and Internal Medicine, Dr. Jan Biziel University Hospital No. 2 in Bydgoszcz, Bydgoszcz PL 85-168, Poland.
authors.forename: Jacek
authors.initials: J
authors.lastname: Fabisiak
authors.affiliation: Clinic of Vascular and Internal Medicine, Dr. Jan Biziel University Hospital No. 2 in Bydgoszcz, Bydgoszcz PL 85-168, Poland.
authors.forename: Karol
authors.initials: K
authors.lastname: Suppan
authors.affiliation: Clinic of Vascular and Internal Medicine, Dr. Jan Biziel University Hospital No. 2 in Bydgoszcz, Bydgoszcz PL 85-168, Poland.
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Pulkowski
authors.affiliation: Department of Pathophysiology, Faculty of Pharmacy, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Bydgoszcz PL 85-094, Poland.
authors.forename: Danuta
authors.initials: D
authors.lastname: Rość
mesh_terms: D000368:Aged; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D003925:Diabetic Angiopathies / Q000097:blood*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000097:blood*; D042461:Vascular Endothelial Growth Factor A / Q000097:blood*; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000097:blood*
chemical_list: C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2
keywords: Angiogenesis; Peripheral arterial disease; Soluble receptors; Type 2 diabetes mellitus; Vascular endothelial growth factor