Epigenetic silencing of the ANKRD26 gene correlates to the pro-inflammatory profile and increased cardio-metabolic risk factors in human obesity.

ABSTRACT:

Background

Obesity is a major worldwide threat to human health. Increasing evidence indicates that epigenetic modifications have a major impact on the natural history of this disorder. Ankyrin Repeat Domain 26 (Ankrd26) is involved in the development of both obesity and diabetes in mice and is modulated by environmentally induced epigenetic modifications. This study aims at investigating whether impaired ANKRD26 gene expression and methylation occur in human obesity and whether they correlate to the phenotype of these subjects.

Results

We found that downregulation of ANKRD26 mRNA and hyper-methylation of a specific region of the ANKRD26 promoter, embedding the CpG dinucleotides - 689, - 659, and - 651 bp, occur in peripheral blood leukocytes from obese compared with the lean

SUBMITTER: Desiderio A 

PROVIDER: S-EPMC6894277 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature