Functional dissection of metabolic trait-associated variants in steady state and stimulated human skeletal muscle cells

Metabolic diseases including type 2 diabetes are caused by genetic and environmental factors. Here, we used a massively parallel reporter assay (MPRA) to characterize the regulatory activity of T2D-associated variants in a human skeletal muscle cell line at basal and multiple stimulatory states. We also performed bulk transcriptomics to identify gene expression signatures across these perturbation conditions.