Objective: Offspring of women with a history of gestational diabetes mellitus (GDM) is at a significantly increased risk of developing obesity and diabetes· It is suggested that intrauterine hyperglycemia can induce epigenetic changes in the fetus which might have a detrimental effect on future metabolic phenotypes· In this study, we compared pairwise DNA methylation status between siblings whose intrauterine exposure to maternal GDM are discordant· Methods: A total of 19 sib-pairs born to 18 Korean women who experienced both normal pregnancy and GDM pregnancy were included· DNA was extracted from peripheral leukocytes when the offspring was at the age between 4 and 15 years· An epigenome-wide association study was conducted using Illumina Infinium HumanMethylation 450 BeadChip assays· Results: In the unsupervised clustering based on Manhattan distance, 33 samples were closely related to intrauterine GDM status· A total of six CpG sites were differentially methylated within sib-pairs with false discovery rate of less than 0·1 ( P < 1·50 × 10-6)· The six sites were located in MFHAS1, LOC92973, PACRG, HNF4A, PITPNM3, and RREB1· Among these CpG sites, cg08407434 which is located at HNF4A was consistently hypermethylated in the offspring of GDM with mean pairwise difference methylation of 1·3% (p = 9·10 × 10-7)· Using Ingenuity Pathway Analysis of differentially methylated regions, we found that immune response was overrepresented by hypermethylated genes· Conclusion: To the best of our knowledge, this is the first study to investigate the epigenome-wide difference in methylation within sib-pairs discordant for intrauterine hyperglycemia· We found several suggestive CpG sites with differential methylation, including the one located in HNF4A which warrants further investigation·