title: Increased oxidative DNA damage in lean normoglycemic offspring of type 2 diabetic patients.
abstract: OBJECTIVE
  Several studies have shown increased oxidative stress in patients with pre-diabetes and newly diagnosed Type 2 diabetes mellitus (T2DM). It has been proposed that oxidative stress initiates insulin resistance in genetically predisposed individuals. The aim of this study was to evaluate the markers of oxidative stress in the offspring of patients with T2DM.
  
  
  METHODS
  We examined 60 lean normoglycemic offspring of Type 2 diabetics, and 52 age, sex and body mass index matched subjects without family history of T2DM as controls. Anthropometric, biochemical and carotid intima media thickness (IMT) measurements and oral glucose tolerance test (OGTT) were performed. Erythrocyte superoxide dismutase and glutathione peroxidase activities, serum nitric oxide, plasma total sulfhydryl (tSH) groups, plasma total antioxidant status, plasma malondialdehyde and serum 8-hydroxydeoxy-guanosine (8-OHdG) levels were compared between 2 groups.
  
  
  RESULTS
  2 groups were similar for the measurements of anthropometric, blood pressure, lipids, fasting glucose, HOMA-IR and carotid IMT. Glucose levels during OGTT were significantly higher in the offspring of Type 2 diabetics than controls (p=0.035). The offspring of Type 2 diabetics showed a significant increase in serum 8-OHdG level (p=0.005) and plasma tSH groups (p=0.032) when compared to the controls. Significant differences were not obtained in other oxidative stress marker levels between 2 groups.
  
  
  CONCLUSIONS
  Main finding of our study was the presence of increased oxidative DNA damage in lean normoglycemic offspring of Type 2 diabetic patients. There is a need for further clinical studies in order to explain whether oxidative stress is present in genetically predisposed subjects and induces the insulin resistance.
authors.affiliation: Ege University Medical School, Endocrinology and Metabolism, Izmir, Turkey. aliyezengi@yahoo.com
authors.forename: A
authors.initials: A
authors.lastname: Zengi
authors.forename: G
authors.initials: G
authors.lastname: Ercan
authors.forename: O
authors.initials: O
authors.lastname: Caglayan
authors.forename: S
authors.initials: S
authors.lastname: Tamsel
authors.forename: M
authors.initials: M
authors.lastname: Karadeniz
authors.forename: I
authors.initials: I
authors.lastname: Simsir
authors.forename: E
authors.initials: E
authors.lastname: Harman
authors.forename: C
authors.initials: C
authors.lastname: Kahraman
authors.forename: M
authors.initials: M
authors.lastname: Orman
authors.forename: S
authors.initials: S
authors.lastname: Cetinkalp
authors.forename: G
authors.initials: G
authors.lastname: Ozgen
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics*; D005192:Family Health; D005260:Female; D020022:Genetic Predisposition to Disease; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D018384:Oxidative Stress; D010290:Parents; D011236:Prediabetic State / Q000097:blood*; D013438:Sulfhydryl Compounds / Q000097:blood; D013851:Thinness / Q000097:blood*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D013438:Sulfhydryl Compounds; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine