title: Peripheral blood mitochondrial DNA content and dysregulation of glucose metabolism.
abstract: OBJECTIVE
  The aim of this study was to examine the potential influence of insulin resistance (IR), hyperglycemia and oxidative stress on leucocytes mitochondrial DNA (mtDNA) content.
  
  
  METHODS
  One hundred twenty-five T2DM, 101 IFG and 70 normal subjects were enrolled in this study. The quantity of relative mtDNA content was measured by a real-time PCR and corrected by simultaneous measurement of the nuclear DNA. Parameters of lipid peroxidation, thiobarbituric acid reactive substance (TBARS), and total free thiols as antioxidative status were measured from serum samples. IR was assessed by homeostasis model assessment in the non-diabetic groups. Relationships among different variables were analyzed by general linear model correlation.
  
  
  RESULTS
  In all subjects, after correcting for age, sex and BMI, there were progressive increases of leucocyte mtDNA copy number, TBARS, and total reduced thiols with progressive dysregulation of glucose metabolism (normal vs. IFG vs. T2DM). Furthermore, correlation between mtDNA content and glucose dysregulation persisted after sequential correction for age, sex, BMI and TBARS. The independent predictor of mtDNA content by regression analysis was hyperglycemia. In non-diabetic group, influence of family history of diabetes on mtDNA content turned to non-significant after correcting for fasting plasma glucose (FPG). Correlation study revealed that mtDNA content was correlated with FPG (P<0.001), but not IR.
  
  
  CONCLUSIONS
  Our results indicate that hyperglycemia, not IR, is associated with an increase of leucocyte mtDNA copy number in cases of glucose dysregulation.
authors.affiliation: Division of Metabolism, Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chang Gung University College of Medicine, Niao-sung Hsiang, Kaohsiung Hsien 83305, Taiwan.
authors.forename: Shao-Wen
authors.initials: SW
authors.lastname: Weng
authors.forename: Tsu-Kung
authors.initials: TK
authors.lastname: Lin
authors.forename: Chia-Wei
authors.initials: CW
authors.lastname: Liou
authors.forename: Shang-Der
authors.initials: SD
authors.lastname: Chen
authors.forename: Yau-Huei
authors.initials: YH
authors.lastname: Wei
authors.forename: Hsin-Chen
authors.initials: HC
authors.lastname: Lee
authors.forename: I-Ya
authors.initials: IY
authors.lastname: Chen
authors.forename: Ching-Jung
authors.initials: CJ
authors.lastname: Hsieh
authors.forename: Pei-Wen
authors.initials: PW
authors.lastname: Wang
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004272:DNA, Mitochondrial / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D007962:Leukocytes / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004272:DNA, Mitochondrial; D017392:Thiobarbituric Acid Reactive Substances; D005947:Glucose