Abstract
Gestational Diabetes Mellitus (GDM) has a high incidence of pregnancy, which seriously affects the life quality of pregnant women and fetal health. DNA methylation is one of the most important epigenetic modification that can regulate the gene expression level, and thus affect the occurrence of various diseases. Increasing evidence has shown that gene expression changes caused by DNA methylation play an important role in metabolic diseases. Here we explored the mechanisms and biological processes that affect the occurrence and development of GDM through analyzing the gene expression profiles and DNA methylation data of GDM. We detected 24,577 differential CpG sites mapping to 9339 genes (DMGs, differential methylation gene) and 931 differential expressed genes (DEGs) between normal samples and GDM samples. GO (gene ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis of 326 overlapping genes between DMGs and DEGs showed obvious enrichment in terms related to metabolic disorders and immune responses. We identified Oas1, Ppie, Polr2g as possible pathogenic target genes of GDM by combining protein-protein interaction analysis. Our study provides possible targets for early diagnosis of GDM and information for clinical prevention of abnormal fetal development and type 2 diabetes.
Highlights
The methyl donor for DNA methylation is the intermediate product of one-carbon metabolism, and increasing evidence have shown that DNA methylation can response to nutritional and environmental influences and www.nature.com/scientificreports/
Genome-wide methylome and transcriptome analysis in hepatocyte isolated from normal people and patients with type 2 diabetes revealed that genes involved in hepatic glycolysis and insulin re-sistance were abnormally hypomethylated and overexpressed in liver14.it is reasonable to speculate that the placenta, as a peripheral tissue susceptible to metabolic disorders, its DNA methylation regulation plays an important role in the pathology
Gestational Diabetes Mellitus (GDM) patients are with higher risk to develop type 2 diabetes than pregnant women with normal blood glucose levels in the future[22]
Summary
The methyl donor for DNA methylation is the intermediate product of one-carbon metabolism, and increasing evidence have shown that DNA methylation can response to nutritional and environmental influences and www.nature.com/scientificreports/. DNA methylome changes were recognized as a faithful readout in tis-sues such as skeletal muscle and adipose in obese people with metabolic abnormalities[12,13]. Genome-wide methylome and transcriptome analysis in hepatocyte isolated from normal people and patients with type 2 diabetes revealed that genes involved in hepatic glycolysis and insulin re-sistance were abnormally hypomethylated and overexpressed in liver[14].it is reasonable to speculate that the placenta, as a peripheral tissue susceptible to metabolic disorders, its DNA methylation regulation plays an important role in the pathology. We confirmed genes related to immune response and metabolic pathways were differentially expressed between healthy gestational women and women with GDM. Differences in expression profile were regulated at least in a great part by DNA methylation level according to our comprehensive DNA methylome studies.
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