Bisphenol-A (BPA) is a ubiquitously present endocrine disrupting chemical, and prenatal exposure produces long-term metabolic dysfunction in the offspring. In female sheep, prenatal BPA induces peripheral insulin resistance with tissue-specific changes in negative mediators of insulin resistance. In skeletal muscle this is manifested as increased oxidative stress markers, triglyceride accumulation, and reduced antioxidant gene expression. To identify changes in gene expression and potential biomarkers of metabolic disruptions, RNA expression was compared in skeletal muscle from prenatal BPA-treated (daily subcutaneous injections of 0.5mg/kg/day BPA in corn oil from days 30 and 90 of gestation (term 147 days)) and control females (corn oil injections for same duration). Prenatal BPA dysregulated 112 genes (32 downregulated and 80 upregulated) at false discovery rate adjusted p value (FDR) <0.05 and absolute log2 fold change>0.5. Gene enrichment analysis showed that prenatal BPA dysregulated 194 gene pathways at FDR<0.01, including pathways related to RNA biosynthetic process, immune function, and collagen synthesis. Orthogonal Projections to Latent Structures Discriminant Analysis identified potential biomarkers of prenatal BPA exposure including downregulation of calpastatin (CAST), nitric oxide synthase 1 (NOS1), deoxyribose-phosphate aldolase (LOC101105149), serum amyloid A protein (LOC101120204) and upregulation of Fas apoptotic inhibitory molecule (FAIM), fatty acid synthase (FASN), DENN domain containing 2B (ST5), family with sequence similarity 71 member A (FAM71A), and arylsulfatase D (LOC101116024). Downregulation of the antioxidant NOS1 and upregulation of the lipid synthesis gene FASN are in line with the increased oxidative stress and lipid accumulation in the muscle from prenatal BPA-treated sheep. Further investigation of the mechanisms by which these biomarkers play a role in the overall functional phenotype will help understand the complex effects of prenatal BPA exposure on metabolism.