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Pathophysiology/Complications

Monocyte Telomere Shortening and Oxidative DNA Damage in Type 2 Diabetes

  1. Mike J. Sampson, MD1,
  2. Mark S. Winterbone, BSC2,
  3. Jackie C. Hughes, BSC2,
  4. Nicoletta Dozio, PHD1 and
  5. David A. Hughes, PHD2
  1. 1Bertram Diabetes Research Unit, Norfolk and Norwich University Hospital National Health Service Trust, Norwich, U.K.
  2. 2Institute of Food Research, Norwich Research Park, Norwich, U.K.
  1. Address correspondence and reprint requests to Dr. Mike Sampson, Elsie Bertram Diabetes Centre, NorfolkNorwich University Hospital National Health Service Trust, Norwich NR4 7UA, U.K. E-mail: mike.sampson{at}nnuh.nhs.uk
Diabetes Care 2006 Feb; 29(2): 283-289. https://doi.org/10.2337/diacare.29.02.06.dc05-1715
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    Figure 1—

    Relationship between oxidative DNA damage and telomere length in type 2 diabetes PBMCs and lymphocytes. Data shown for 21 type 2 diabetic patients for all PBMCs (upper panel), naïve T-cells (middle panel), and memory T-cells (lower panel). MESF by flow-fluorescent in situ hybridization and DNA damage by flow cytometry of 8-oxoguanine as described in text. Regression line and 95% CI for regression shown.

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  • Table 1—

    Clinical features of type 2 diabetes and control groups

    Control subjectsType 2 diabetes
    n2821
    Age (years)61.2 ± 5.362.0 ± 5.6
    Diabetes duration (years)—3.0 (6.5)
    Waist-to-hip ratio0.92 ± 0.040.93 ± 0.07
    BMI (kg/m2)17.3 ± 3.329.5 ± 3.6*
    Fasting plasma glucose (mmol/l)4.9 ± 0.59.1 ± 2.5†
    Fasting plasma insulin (mU/l)58.4 ± 3051.8 ± 21
    2-h plasma glucose (mmol/l)5.8 ± 1.417.7 ± 4†
    2-h plasma insulin (mU/l)305 ± 230170 ± 127*
    HOMA-insulin resistance13.0 ± 721.1 ± 10*
    A1C (%)5.4 ± 0.37.9 ± 1.5†
    Systolic blood pressure (mmHg)140 ± 19141 ± 14
    Diastolic blood pressure (mmHg87 ± 1182 ± 6
    Plasma total cholesterol (mmol/l)5.4 ± 0.84.7 ± 0.7*
    Plasma HDL cholesterol (mmol/l)1.3 ± 0.41.1 ± 0.3*
    Plasma tryiglycerides (mmol/l)1.3 ± 0.71.8 ± 1.6
    Plasma LDL cholesterol (mmol/l)3.5 ± 0.72.2 ± 0.6†
    hsCRP (μg/l)905 (969)801 (1,045)
    • Data are means ± SD or median (interquartile range); all study subjects were male and receiving no medication.

    • *

      ↵* P < 0.05;

    • †

      ↵† P < 0.0001.

  • Table 2—

    Telomere length and oxidative DNA damage in subjects with or without type 2 diabetes

    Control subjectsType 2 diabetesP
    n2821
    Telomere length
        PBMC8.9 ± 3.17.3 ± 2.50.062
        Naïve T-cells8.7 ± 3.08.1 ± 2.70.53
        Memory T-cells7.4 ± 2.97.0 ± 2.40.60
        Monocytes5.5 ± 1.14.0 ± 1.10.0001
    Oxidative DNA damage
        PBMC442 ± 86483 ± 960.12
        Naïve T-cells390 ± 106447 ± 1170.07
        Memory T-cells473 ± 70508 ± 930.14
    • Data are means ± SD. Data as MESF for telomere length and mean fluorescent intensity for 8-oxoguanine as a marker of oxidative DNA damage. Monocyte-specific DNA damage was not measurable.

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Diabetes Care: 29 (2)

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February 2006, 29(2)
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Monocyte Telomere Shortening and Oxidative DNA Damage in Type 2 Diabetes
Mike J. Sampson, Mark S. Winterbone, Jackie C. Hughes, Nicoletta Dozio, David A. Hughes
Diabetes Care Feb 2006, 29 (2) 283-289; DOI: 10.2337/diacare.29.02.06.dc05-1715

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Monocyte Telomere Shortening and Oxidative DNA Damage in Type 2 Diabetes
Mike J. Sampson, Mark S. Winterbone, Jackie C. Hughes, Nicoletta Dozio, David A. Hughes
Diabetes Care Feb 2006, 29 (2) 283-289; DOI: 10.2337/diacare.29.02.06.dc05-1715
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