EPIGENETIC ALTERATIONS IN PATIENTS
WITH TYPE 2 DIABETES MELLITUS Karachanak-Yankova S1,a, Dimova R2,a, Nikolova D1, Nesheva D1, Koprinarova M3,
Maslyankov S4, Tafradjiska R5, Gateva P6, Velizarova M7, Hammoudeh Z1, Stoynev N2,
Toncheva D1, Tankova T2, Dimova I1,* *Corresponding Author: Ivanka Dimova, Associate Professor, Department of Medical Genetics, Medical University
Sofia, Zdrave str. 2, 1431 Sofia, Bulgaria. Tel: +359-2-91-72-735. E-mail: ivanka.i.dimova@ gmail.com page: 15 download article in pdf format
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Abstract
Epigenetic changes, in particular DNA methylation
processes, play a role in the pathogenesis
and progression of type 2 diabetes mellitus (T2DM)
linking genetic and environmental factors. To clarify
this role, we have analyzed in patients with different
duration of T2DM: (i) expression levels of methyl-
CpG-binding domain protein 2 (MBD2) as marker
of DNA methylation, and ii) methylation changes
in 22 genes connected to cellular stress and toxicity.
We have analyzed MBD2 mRNA expression levels
in 16 patients and 12 controls and the methylation
status of stress and toxicity genes in four DNA pools:
(i) controls; (ii) newly-diagnosed T2DM patients;
(iii) patients with T2DM duration of <5 years and
(iv) of >5 years. The MBD2 expression levels were
10.4-times increased on average in T2DM patients
compared to controls. Consistent increase in DNA
methylation fraction with the increase in T2DM duration
was observed in Prdx2 and SCARA3 genes, connected
to oxidative stress protection and in BRCA1
and Tp53 tumor-suppressor genes. In conclusion,
increased MBD2 expression in patients indicated general
dysregulation of DNA methylation in T2DM. The
elevated methylation of Prdx2 and SCARA3 genes
suggests disturbance in oxidative stress protection
in T2DM. The increased methylation of BRCA1 and
Tp53 genes unraveled an epigenetic cause for T2DM
related increase in cancer risk.
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