title: Plasma total homocysteine levels and methylenetetrahydrofolate reductase gene polymorphism in patients with type 2 diabetes mellitus.
abstract: BACKGROUND
  Thrombotic episodes account for approximately 80% of deaths in type 2 diabetic patients. Hyperhomocysteinaemia is a well recognized independent risk factor for atherosclerosis and thromboembolism. Increased homocysteine levels may occur due to a number of factors including inherited gene polymorphism of methylenetetrahydrofolate reductase (MTHFR) C677T. Here, we evaluate plas- ma total homocysteine (tHcy) levels and frequency of the MTHFR C677T gene polymorphism in asymptomatic healthy volunteers and type 2 diabetic patients with hypertension but without nephropathy. We have also investigated the relationship between tHcy levels and the presence of MTHFR C677T gene polymorphism.
  
  
  METHODS
  Plasma tHcy levels and MTHFR C677T genotype were investigated in a total of 53 subjects. These included asymptomatic healthy volunteers (n = 16), patients with type 2 diabetes (n = 7), subjects with hypertension (n = 12) and patients with both type 2 diabetes and hypertension (n = 18). Renal function, serum lipids and other metabolites were also assessed.
  
  
  RESULTS
  There was no significant difference in tHcy levels between the groups studied. The frequency of MTHFR C677T gene polymorphism observed was similar to that obtained for the general Brazilian population. In patients with type 2 diabetes and hypertension but without impaired renal function, we observed no meaningful correlation between increased tHcy levels and the presence of MTHFR C677T gene polymorphism.
  
  
  CONCLUSIONS
  Type 2 diabetics who are homozygous or heterozygous for the MTHFR C677T gene polymorphism showed normal tHcy levels. Our results further suggest that diabetes without an associated adverse risk profile is not an independent correlate of increased tHcy levels.
authors.affiliation: Faculty of Pharmacy, Federal University of Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Anna L
authors.initials: AL
authors.lastname: Soares
authors.forename: Ana P
authors.initials: AP
authors.lastname: Fernandes
authors.forename: Jarbas E
authors.initials: JE
authors.lastname: Cardoso
authors.forename: Marinez O
authors.initials: MO
authors.lastname: Sousa
authors.forename: Marcelo C
authors.initials: MC
authors.lastname: Lasmar
authors.forename: Bethânia A
authors.initials: BA
authors.lastname: Novelli
authors.forename: Geralda F
authors.initials: GF
authors.lastname: Lages
authors.forename: Luci M
authors.initials: LM
authors.lastname: Dusse
authors.forename: Lauro M
authors.initials: LM
authors.lastname: Vieira
authors.forename: Bashir A
authors.initials: BA
authors.lastname: Lwaleed
authors.forename: Maria G
authors.initials: MG
authors.lastname: Carvalho
mesh_terms: D000328:Adult; D001938:Brazil; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005260:Female; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000235:genetics*; D006973:Hypertension; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics*; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide
chemical_list: D006710:Homocysteine; D042965:Methylenetetrahydrofolate Reductase (NADPH2)