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Genomic damage in patients with type-2 diabetes mellitus

D N Binici1, A Karaman, M Coşkun

  • 1Department of Internal Medicine, Erzurum Training and Research Hospital, Erzurum, Turkey.

Genetic Counseling (Geneva, Switzerland)
|September 17, 2013
PubMed

Insights

Type-2 diabetes mellitus (DM2) is linked to increased DNA damage, specifically higher frequencies of sister chromatid exchange (SCE) and micronuclei (MN). This genomic instability in DM2 patients may stem from hyperglycemia-induced oxidative stress.

Area of Science:

  • Genetics
  • Endocrinology
  • Molecular Biology

Background:

  • DNA damage is implicated in the pathogenesis of type-2 diabetes mellitus (DM2) and its complications.
  • Various in vitro assays exist for measuring DNA damage.

Purpose of the Study:

  • To investigate the frequency of sister chromatid exchange (SCE) and micronuclei (MN) in DM2 patients compared to healthy controls.

Main Methods:

  • Blood cell cultures from 50 DM2 patients and 30 healthy controls were analyzed.
  • Sister chromatid exchange (SCE) and micronuclei (MN) tests were performed.
  • Demographic and clinical data, including HbA1c levels, were collected.

Main Results:

  • DM2 patients exhibited significantly higher frequencies of SCE (7.11 +/- 1.14) compared to controls (4.96 +/- 0.92) (p < 0.001).
  • SCE frequency positively correlated with HbA1c levels (p < 0.05) but not with diabetes duration.
  • A significant increase in MN frequency was observed in DM2 patients (3.45 +/- 1.01 per 1000 cells) versus controls (1.79 +/- 0.67 per 1000 cells) (p < 0.001).
  • No significant correlation was found between MN frequency and diabetes duration or HbA1c levels.

Conclusions:

  • DM2 is characterized by genomic instability, evidenced by elevated SCE and MN frequencies.
  • Hyperglycemia-induced oxidative stress is a potential underlying mechanism for increased DNA damage in DM2.
  • These findings highlight the role of DNA damage in DM2 pathogenesis and complications.

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