Insulin plays a central role in metabolic control, and its downstream signaling can modulate transcription, RNA splicing, isoform usage, and RNA modifications such as m6A. There is a mounting assortment of reported evidence supporting RNA modifications as a key mode of regulation in adipocytes which have been found to be involved in processes such as metabolism, inflammation, and disease. However, such studies have focused on individual epitranscriptomic regulators and their involvement in cellular function, failing to capture a broader epitranscriptome-centric regulatory landscape in adipocytes. Here we aim to investigate the roles of RNA modifications in insulin signaling and how epitranscriptomic aberrations can contribute to insulin resistance. Further, we are interested and hopeful in exploring the adipocyte epitranscriptome as a potential axis of therapeutic intervention for insulin resistance. This project involves the analysis of direct RNA sequencing data generated from 24 human samples sequenced with the recently commercially released RNA004 chemistry from Oxford Nanopore Technologies collected under insulin stimulated conditions and as unstimulated controls. To study RNA modifications’ role in insulin resistance, our data includes white adipose tissue derived from 4 human patients that transition from an insulin resistant to an insulin sensitive state post bariatric surgery. Samples included were collected 0 and 5 years post bariatric surgery, before and after hyperinsulinemic-euglycemic clamp for a total of 16 individual datasets. Main deliverables of the planned analysis will include determination of statistically significant differential RNA modification and an epitranscriptomic map of the adipocyte cell in an insulin starved and an insulin stimulated state.