Obesity impairs reproductive functions through multiple mechanisms, possibly through disruption of ovarian function. We hypothesized that increased adiposity will lead to a pro-inflammatory gene signature and up-regulation of Egr-1 protein in ovaries from obese (OB, n=7) compared to lean (LN, n=10) female Sprague Dawley rats during the peri-implantation period at 4.5 days post-coitus (dpc). Obesity was induced by overfeeding (40% excess calories for 28 d) via total enteral nutrition prior to mating. OB dams had higher body weight (p<0.001), greater fat mass (p<0.001), reduced lean mass (p<0.05), and developed metabolic dysfunction with elevated serum lipids, insulin, leptin, and CCL2 (p<0.05) compared to LN dams. Microarray analyses identified 284 differentially-expressed genes between ovaries from LN vs. OB dams (±1.3 fold, p<0.05). RT-qPCR confirmed a decrease in expression of glucose transporters GLUT4 and GLUT9 and elevation of pro-inflammatory genes including CCL2, CXCL10, CXCL11, CCR2, CXCR1, and TNF-α in ovaries from OB compared to LN (p<0.05). Protein levels of PI3K and phosphorylated AKT were significantly decreased (p<0.05) while nuclear levels of Egr-1 (p<0.05) were increased in OB compared to LN ovaries. Moreover, Egr-1 was localized to granulosa cells, with highest expression in cumulus cells of pre-ovulatory follicles. mRNA expression of VCAN, AURKB and PLAT (p<0.05) correlated with %visceral fat weight (r=0.51, -0.77, and -0.57, p<0.05, respectively), suggesting alterations in ovarian function with obesity. In summary, maternal obesity led to an up-regulation of inflammatory genes and Egr-1 expression in peri-implantation ovarian tissue, and a concurrent down-regulation of GLUTs and AKT and PI3K protein levels.