title: Serum visfatin and its relation to insulin resistance and inflammation in type 2 diabetic patients with and without macroangiopathy.
abstract: OBJECTIVE
  To explore visfatin levels and its relationship to obesity, insulin resistance, lipid profile and inflammation in type 2 diabetes mellitus (T2DM) patients with and without macroangiopathy.
  
  
  METHODS
  The study was designed in the College of Medicine, Qassim University, Qassim, Kingdom of Saudi Arabia, and implemented between April 2006 and May 2007. It involved 84 subjects divided into 3 groups: 29 T2DM patients without macroangiopathy, 33 T2DM patients with macroangiopathy, and 22 non-diabetic controls. After overnight fast, weight, height, and blood pressure were measured and a single blood sample was obtained. Serum visfatin, insulin, interleukin-6 (IL-6), and high sensitive C-reactive protein (hsCRP) were measured by Enzyme-linked immunosorbent assay (ELISA), whereas glucose and lipid profile were measured using colorimetric enzymatic methods. Obesity was measured using body mass index (BMI) and insulin resistance was measured using Homeostasis Model Assessment-Insulin Resistance (HOMA-IR).
  
  
  RESULTS
  Compared to control, both non-macroangiopathic and macroangiopathic diabetic groups were associated significantly with an atherogenic lipid profile, and high levels of glucose, insulin, HOMA-IR, hsCRP and IL-6. Serum visfatin was significantly higher in non-complicated diabetics compared to controls and macroangiopathic diabetics, but difference in visfatin level between macroangiopathic diabetics and controls was insignificant. Visfatin levels were not correlated with BMI, insulin, glucose, or HOMA-IR, but they were negatively and significantly correlated with hsCRP, IL-6, and the atherogenicity of lipid profile.
  
  
  CONCLUSIONS
  Visfatin levels were increased in T2DM regardless of BMI and type of diabetic treatment. These levels were correlated negatively with inflammatory markers and atherogenicity of lipid profile.
authors.affiliation: Department of Pharmacology and Therapeutics, College of Medicine, Qassim University, PO Box 6040, Al-Mlaida 51442, Kingdom of Saudi Arabia. ghasham@ksu.edu.sa
authors.forename: Abdullah A
authors.initials: AA
authors.lastname: Alghasham
authors.forename: Youssef A
authors.initials: YA
authors.lastname: Barakat
mesh_terms: D000328:Adult; D000789:Angina, Unstable / Q000097:blood*; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000145:classification; D003925:Diabetic Angiopathies / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D020521:Stroke / Q000097:blood*; D014652:Vascular Diseases / Q000097:blood*
chemical_list: D007328:Insulin; D015850:Interleukin-6; D008055:Lipids; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase