Research article

Lack of association of colonic epithelium telomere length and oxidative DNA damage in Type 2 diabetes under good metabolic control

Deepak Kejariwal¹ , Karolina M Stepien^{* 2} , Tracy Smith^{* 3} , Hugh Kennedy^{* 1} , David A Hughes^{* 3} and Mike J Sampson^{* 2}

¹Department of Gastroenterology, Norfolk and Norwich University Hospital Colney Lane, Norwich NR4 7UY, UK

²Elsie Bertram Diabetes Centre, Norfolk and Norwich University Hospital, Norwich NR4 7UA, UK

³Institute of Food Research, Norwich Research Park, Colney, Norwich NR4 7UA, UK

author email corresponding author email* Contributed equally

BMC Endocrine Disorders 2008, 8:12doi:10.1186/1472-6823-8-12

Published:	10 October 2008

Abstract

Background

Telomeres are DNA repeat sequences necessary for DNA replication which shorten at cell division at a rate directly related to levels of oxidative stress. Critical telomere shortening predisposes to cell senescence and to epithelial malignancies. Type 2 diabetes is characterised by increased oxidative DNA damage, telomere attrition, and an increased risk of colonic malignancy. We hypothesised that the colonic mucosa in Type 2 diabetes would be characterised by increased DNA damage and telomere shortening.

Methods

We examined telomere length (by flow fluorescent in situ hybridization) and oxidative DNA damage (flow cytometry of 8 – oxoguanosine) in the colonic mucosal cells of subjects with type 2 diabetes (n = 10; mean age 62.2 years, mean HbA1c 6.9%) and 22 matched control subjects. No colonic pathology was apparent in these subjects at routine gastrointestinal investigations.

Results

Mean colonic epithelial telomere length in the diabetes group was not significantly different from controls (10.6 [3.6] vs. 12.1 [3.4] Molecular Equivalent of Soluble Fluorochrome Units [MESF]; P = 0.5). Levels of oxidative DNA damage were similar in both T2DM and control groups (2.6 [0.6] vs. 2.5 [0.6] Mean Fluorescent Intensity [MFI]; P = 0.7). There was no significant relationship between oxidative DNA damage and telomere length in either group (both p > 0.1).

Conclusion

Colonic epithelium in Type 2 diabetes does not differ significantly from control colonic epithelium in oxidative DNA damage or telomere length. There is no evidence in this study for increased oxidative DNA damage or significant telomere attrition in colonic mucosa as a carcinogenic mechanism.