title: Apolipoprotein E polymorphism in diabetic and non-diabetic patients: does it really contribute to atherosclerosis?
abstract: OBJECTIVE
  The exact mechanism of the increased cardiovascular morbidity and mortality in type-2 diabetes is still undefined. The aim of our study was to assess the impact of apolipoprotein E (apo E) polymorphism and other factors on atherosclerotic vascular disease in type-2 diabetic patients. We also examined the association between apo E polymorphism and lipid profile in diabetic patients.
  
  
  RESULTS
  We assessed the apo E polymorphism in 295 atherosclerotic patients (124 of them had diabetes (according to WHO criteria) and 171 of them had coronary artery narrowing > 50). The detection of apo E polymorphism was made by Real-Time PCR using a Light-Cycler (Roche diagnostics, GmbH, Mannheim, Germany). Serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), lipoprotein (a) [Lp(a)], apolipoprotein A (Apo A) and apolipoprotein B (Apo B) levels were determined by biochemical analyser. Genotypic distribution of apo E polymorphism did not differ between diabetic and non-diabetic atherosclerotic patients. The distributions of apo E2/2, E2/3, E2/4, E3/3, E3/4 and E4/4 genotypes in diabetic and non-diabetic atherosclerotic patients were 7.3%: 8.2%, 15.3%: 15.8%, 4.0%: 5.3%, 50.8%: 56.7%, 16.9%: 11.1% and 5.6%: 2.9%, respectively. Participants were grouped as apo E2 (E2/2 or E2/3), apo E3 (E3/3), or apo E4 (E4/4 or E4/3). The distributions of apo E2, E3 and E4 alleles were 23.5%, 52.9%, 23.5%, for diabetic patients, and 25.3%, 59.9%, 14.8% for non-diabetic patients, respectively. The apolipoprotein E genotype was not associated with the lipid levels in diabetic patients.
  
  
  CONCLUSIONS
  Our findings imply that apo E polymorphism is not related to the development of atherosclerosis in patients with type-2 diabetes.
authors.affiliation: Department of Cardiology, Mersin University, Turkey.
authors.forename: Ahmet
authors.initials: A
authors.lastname: Camsari
authors.forename: Lülüfer
authors.initials: L
authors.lastname: Tamer
authors.forename: Nurcan
authors.initials: N
authors.lastname: Aras Ateş
authors.forename: Hasan
authors.initials: H
authors.lastname: Pekdemir
authors.forename: Dilek
authors.initials: D
authors.lastname: Ciçek
authors.forename: Bahadir
authors.initials: B
authors.lastname: Ercan
authors.forename: Handan
authors.initials: H
authors.lastname: Camdeviren
authors.forename: Ugur
authors.initials: U
authors.lastname: Atik
mesh_terms: D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000235:genetics; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000235:genetics / Q000378:metabolism; D005260:Female; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D001057:Apolipoproteins E; D008055:Lipids; D008074:Lipoproteins; D002784:Cholesterol