Global DNA methylation and homocysteine levels are lower in type 1 diabetes patients

被引:6
|
作者
Arroyo-Jousse, Vivian [1 ,2 ]
Garcia-Diaz, Diego F. [1 ,3 ]
Perez-Bravo, Francisco [1 ,4 ]
机构
[1] Univ Chile, Fac Med, Dept Nutr, Santiago 7, Chile
[2] Univ Chile, Fac Med, Med Vet, Santiago 7, Chile
[3] Univ Chile, Fac Med, Biotecn, Santiago 7, Chile
[4] Univ Chile, Fac Med, Bioquim, Santiago 7, Chile
关键词
DNA methylation; Epigenetics; Folate; Type; 1; Diabetes; PLASMA HOMOCYSTEINE; METABOLISM; MELLITUS; INSULIN; FOLATE; COMPLICATIONS; EPIGENETICS; ETIOLOGY; SANTIAGO; CHILE;
D O I
10.4067/S0034-98872015000500002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: The worldwide rise in the incidence of Type I Diabetes (T1D), and the concordance rate between monozygotic twins (50%), indicate a strong effect of the environment as an underlying factor of this disease. This process can occur throughout epigenetic modifications of gene expression such as DNA methylation, in which several nutrients participate as cofactors. Aim: To determine DNA methylation status in T1D patients and if it is related to plasma levels of folates and homocysteine (Hcy). Material and Methods: We obtained blood samples from 25 T1D patients aged 13.7 +/- 5.9 years (11 males) and 25 healthy subjects aged 31.1 +/- 7.8 years (16 males). DNA methylation was measured using a colorimetric kit in extracted DNA. Results are expressed as median (interquartile range). Results: Compared with healthy controls, T1D patients had lower global DNA methylation (0.85 (0.91) % and 1.25 (1.16) % respectively, p < 0.02) and Hey levels (4.8 (1.1) ymola and 7.3 (1.4) mu mol/L respectively p < 0.01). There were no differences in folate levels between groups. A significant association between folates and global DNA methylation status was observed in T1D patients (r = -0.564, p < 0.01) and healthy subjects (r = 0.440, p = 0.03). Conclusions: TD1 patients had lower levels of Hcy and global DNA methylation. It is relevant to further investigate if this imbalance also induces epigenetic changes in a gene-specific manner, especially in key genes involved in T1D pathogenesis.
引用
收藏
页码:562 / 568
页数:7
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