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Genome-wide analysis reveals DNA methylation markers that varies with both age and obesity

ABSTRACT: Background: The obesity epidemic and the aging population of many western countries together with their associated diseases are major challenges for the healthcare. As obesity is a risk factor for many age related diseases, such as cancer, it is of importance to understand their interaction and the underlying molecular mechanisms. Lately, epigenetic programming in the form of DNA methylation and have been recognized for its importance in aging, obesity and several diseases. Method: Herein, the methylation level was determined for around 27000 CpG-islands in 46 DNA samples from adult peripheral blood with microarrays. The dependence for each CpG island with age, obesity and their interaction was ascertained with a general linear model. Results: The methylation level of more than 100 genomic sites were significantly altered with increasing age together with 10 additional sites that were differentially methylated with age in obese and lean individuals. The majority of the genomic sites were hypermethylated during aging, including the telomerase catalytic subunit (TERT). However, age dependent hypermethylation was prohibited or reverted in 8 of 10 regions in obese where an interaction between age and obesity was observed. Moreover, one region (LINC00304) was differentially methylated in obese and lean. Conclusion: This study provides evidence for an obesity influence on age driven epigenetic changes, which provide a molecular link between aging and obesity. This link and the identified markers may prove to be valuable biomarkers for the understanding of the molecular basis of aging, obesity and associated diseases.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44763 | GEO | 2014/07/09

SECONDARY ACCESSION(S): PRJNA191639

REPOSITORIES: GEO

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Project description:Background/Objectives: Obese subjects have increased number of enlarged fat cells which are reduced in size but not number in post-obesity. We performed DNA methylation profiling in fat cells with the aim of identifying differentially methylated DNA sites (DMS) linked to adipose hyperplasia (many small fat cells) in post-obesity. Subjects/Methods: Genome-wide DNA methylation was analyzed in abdominal subcutaneous fat cells from 16 women examined two years after gastric bypass surgery at a post-obese state (BMI 26±2 kg/m2, mean±s.d.) and 14 never-obese women (BMI 25±2 kg/m2). Gene expression was analyzed in subcutaneous adipose tissue from 9 women in each group. In a secondary analysis, we examined DNA methylation and expression of adipogenesis genes in 15 and 11 obese women, respectively. Results: The average degree of DNA methylation of all analyzed CpG-sites was lower in fat cells from post-obese as compared to never-obese women (P=0.014). 8,504 CpG sites were differentially methylated in fat cells from post-obese versus never-obese women (false discovery rate 1%). DMS were under-represented in CpG-islands and surrounding shores. The 8,504 DMS mapped to 3,717 unique genes; these genes were over-represented in cell differentiation pathways. Notably, 27% of genes linked to adipogenesis (i.e. 35 of 130) displayed DMS (adjusted P=10−8) in post-obese versus never-obese women. Next, we explored DNA methylation and expression of genes linked to adipogenesis in more detail in adipose tissue samples. DMS annotated to adipogenesis genes were not accompanied by differential gene expression in post-obese compared to never-obese women. In contrast, adipogenesis genes displayed differential DNA methylation accompanied by altered expression in obese women, Conclusions: Global CpG hypomethylation and overrepresentation of DMS in adipogenesis genes in fat cells may contribute to adipose hyperplasia in post-obese women. Post obese=16, Control group=14.

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Genome-wide analysis reveals DNA methylation markers that varies with both age and obesity

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