Skeletal muscle is the primary tissue responsible for insulin resistance and type 2 diabetes (T2D). The fetal stage is crucial for skeletal muscle development. Obesity induces inflammatory responses, which might regulate myogenesis through Wnt/-catenin signaling. The objective of this study was to evaluate the effects of maternal obesity (greater than 30% increase in BMI) during pregnancy on myogenesis, the Wnt/-catenin and inhibitor of B kinase (IKK)/nuclear factor B (NF-B) pathways in fetal skeletal muscle using an obese pregnant sheep model. Non-pregnant ewes were assigned to a control group (C, fed 100% of National Research Council (NRC) recommendations, n = 5) or obesogenic (OB, fed 150% of NRC recommendations, n = 5) diet from 60 days before to 75 days after conception (term ~148 days) when fetal semitendenosus skeletal muscle (St) was sampled for analyses. Myogenic markers including MyoD, myogenin and desmin contents were reduced in OB compared to C fetal St, indicating the down-regulation of myogenesis. The diameter of primary muscle fibers was smaller in OB fetal muscle. Phosphorylation of GSK3 was reduced in OB compared to C fetal St. Though the -Catenin level was lower in OB than C fetal muscle, more -catenin was associated with FOXO3a in the OB fetuses. Moreover, we found phosphorylation levels of IKK and RelA/p65 were both increased in OB fetal muscle. In conclusion, our data showed that myogenesis and the Wnt/-catenin signaling pathway were down-regulated, whereas inflammatory IKK/NF-B signaling pathways were up-regulated in fetal muscle of obese mothers.