title: Inter-relationships between DNA damage, ascorbic acid and glycaemic control in Type 2 diabetes mellitus.
abstract: OBJECTIVE
  The onset of complications in Type 2 diabetes mellitus (DM) patients cannot be predicted in individuals. Evidence suggests a link between complications and hyperglycaemia, oxidative stress and antioxidants, but causality is unclear. This study investigated baseline (entry) fasting plasma ascorbic acid, lymphocytic DNA damage and glycaemic control in Type 2 DM as part of a long-term study, the aim of which is to explore a biomarker profiling approach to identify and improve outcome in high-risk subjects.
  
  
  METHODS
  A cross-sectional study, in which DNA damage, glycated haemoglobin (HbA(1c)), fasting plasma glucose (FPG) and ascorbic acid (AA) were measured on fasting blood samples collected from 427 Type 2 DM subjects.
  
  
  RESULTS
  DNA damage was significantly (P < 0.0001) and directly correlated to both FPG (r = 0.540) and HbA(1c) (r = 0.282), and was significantly (P < 0.0001), independently and inversely correlated to plasma AA (r = -0.449). In those subjects with both poor glycaemic control and low AA (< 48 microm, the overall mean value for the study group), DNA damage was significantly (P < 0.005) higher compared with those subjects with a similar degree of hyperglycaemia but with AA above the mean.
  
  
  CONCLUSIONS
  The novel finding of a significant inverse relationship between plasma AA and DNA damage in Type 2 DM indicates that poorly controlled diabetic subjects might benefit from increased dietary vitamin C. The data also have important implications for biomarker profiling to identify those subjects who might benefit most from intensive therapy. Longer-term follow-up is underway.
authors.affiliation: Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Kowloon, Hong Kong.
authors.forename: S W
authors.initials: SW
authors.lastname: Choi
authors.forename: I F F
authors.initials: IF
authors.lastname: Benzie
authors.forename: C S Y
authors.initials: CS
authors.lastname: Lam
authors.forename: S W S
authors.initials: SW
authors.lastname: Chat
authors.forename: J
authors.initials: J
authors.lastname: Lam
authors.forename: C H
authors.initials: CH
authors.lastname: Yiu
authors.forename: J J
authors.initials: JJ
authors.lastname: Kwan
authors.forename: Y H
authors.initials: YH
authors.lastname: Tang
authors.forename: G S P
authors.initials: GS
authors.lastname: Yeung
authors.forename: V T F
authors.initials: VT
authors.lastname: Yeung
authors.forename: G C
authors.initials: GC
authors.lastname: Woo
authors.forename: B M
authors.initials: BM
authors.lastname: Hannigan
authors.forename: J J
authors.initials: JJ
authors.lastname: Strain
mesh_terms: D001205:Ascorbic Acid / Q000097:blood*; D015415:Biomarkers; D001786:Blood Glucose / Q000032:analysis*; D003430:Cross-Sectional Studies; D004249:DNA Damage / Q000235:genetics*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology
chemical_list: D001205:Ascorbic Acid; D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin