Gestational diabetes mellitus (GDM) is an obstetric disorder affecting approximately 10% of pregnancies. The 4HFHS (High Fat High Sucrose) mouse model emulates GDM in lean women. Dams are fed a HFHS diet one week prior to mating and throughout gestation resulting in inadequate insulin response to glucose in mid-late pregnancy. The offspring of HFHS dams have increased adiposity, thus, we hypothesized that maternal metabolic alterations during lean GDM would compromise ovarian function in offspring both basally and in response to a control or HFHS diet in adulthood. Briefly, D_LP_L were lean dams and control diet pups; D_LP_H were lean dams and HFHS pups; D_HP_L were HFHS dams and control diet pups and D_HP_H were HFHS dams and HFHS pups. A HFHS challenge in the absence of maternal GDM (D_LP_L vs. D_LP_H) increased 3 and decreased 30 ovarian proteins. Maternal GDM in the absence of a dietary stress (D_LP_L vs. D_HP_L) increased abundance of 4 proteins and decreased abundance of 85 proteins in the offspring ovary. Finally, 87 proteins increased, and 4 proteins decreased in offspring ovaries due to dietary challenge and exposure to maternal GDM in utero (D_LP_L vs. D_HP_H). Canopy FGF signaling regulator 2 (CNPY2), Deleted in azoospermia-associated protein 1 (DAZAP1), Septin 7 (SEPT7), and Serine/arginine rich splicing factor 2 (SRSF2) were altered across multiple offspring groups. Together, these findings suggest a possible impact on fertility and oocyte quality in relation to GDM exposure in utero as well as in response to a western diet in later life.