Background: Gestational diabetes mellitus (GDM) is defined as the development of glucose intolerance during pregnancy. It is one of the most common complications of pregnancy, is linked to fetal overgrowth, and predisposes the mother and her child to develop metabolic disease like type-2 diabetes in later life. The placenta is a multifunctional organ that develops during pregnancy and may be central to the pathogenesis and sequalae of GDM, but the metabolic pathways and epigenetic mechanisms possibly involved are not fully understood. This study aimed to perform a systematic review and meta-analysis using existing transcriptome and methylome datasets of the placenta to identify particular types/classes of genes and epigenetic events that may be of significance for understanding the role of placenta in the molecular pathophysiology of GDM.   Methods: We retrieved published transcriptome-wide and methylome-wide studies performed on term human placenta by performing searches on PubMed, Google Scholar, Gene Expression Omnibus and Europe PMC. For inclusion, studies needed to show a list of differentially expressed or methylated genes using high-throughput sequencing technologies or microarray, comparing control and GDM samples. Studies which included participants with other health or pregnancy complications (e.g. pre-existing diabetes and preeclampsia) were excluded. Different R packages such as upsetR, among other Bioconductor packages were used to compare the results between the studies.   Results: We identified 14 studies for assessment. Ten contained a list of differentially expressed (DEG) RNAs between GDM and control placenta and provided pathway analyses. Of the DEGs identified, two were non-coding RNAs. Five studies showed differentially methylated genes. The sample size and number of DEGs between GDM and control placentas varied from 41 to 3 samples per group and from 300 to 20 genes. Genes including CXCL10, CXCL11, GBP1, FABP5, LPL, CFH, LUM, and several encoding HLAs (e.g. HLA-C and HLA-DQA2) were shown to be dysregulated in GDM in more than 3 transcriptome datasets surveyed while MIR30B was consistently altered in the GDM placenta of 2 transcriptome datasets. Biosynthesis, cytokine activity, immune response regulation and oxidative phosphorylation were pathways commonly enriched in the transcriptome studies. In addition, methylation of the TPO, VIPR1, BCAR1, CAPN1 and SEPT9 genes were shown to be aberrant in at least 2 of the surveyed methylome studies. Meta-analysis of the transcriptome and methylome studies identified different intersection sizes between specific studies. Work is underway to correlate transcriptome and methylome datasets.    Conclusion: Overall, the number of studies performed on placenta in GDM concerning RNA, and specifically DNA methylation changes by sequencing is restricted. The overlap between studies is limited, and likely due to variations in participant characteristics including ethnicity, BMI, GDM treatment and diagnosis, as well as offspring sex. However, the overlap of DEGs and differentially methylated genes identified in the current study may inform on the pathogenesis and impact of GDM on maternal and offspring metabolic health. Correlating transcriptome and methylome datasets will provide information of the mechanisms regulating gene expression in the GDM placenta. Future work could also be improved by including maternal and cord blood sequencing data.