Obesity currently affects over one-third of reproductive-age women in the world leading to overall health and metabolic disorders, including reproductive function. Obese women experience subfertility and infertility at greater rates but more importantly, when they do get pregnant, their offspring suffer significant health consequences. Offspring of obese women are more likely than those born to normal-weight women to be obese at one year of age; and to have cardiometabolic sequelae, hypertension, and liver disease as they age. Given the severity and intractability of the obesity epidemic, we must identify effective means of intervention to prevent these detrimental effects of maternal obesity; this requires determination of the underlying mechanisms. In this presentation, using a mouse diet-induced obesity model, I will discuss the rationale for attributing these offspring abnormalities to the maternal oocyte, specifically due to a metabolic aberration originating in the oocyte mitochondria. This phenomenon involves mitochondrial dynamic proteins and mtDNA transcription. Since the maternal oocyte mitochondria are the template for all mitochondria in the offspring, we find this mitochondrial dysfunction in every organ examined in the F1, F2 and F3 generations, suggesting a germline, epigenetic phenomenon. I will also present data to suggest that this process is not reversible by dietary changes or exercise in the mothers. Finally, I will introduce data to support possible mechanisms to explain the transgenerational transfer of these maternal metabolic abnormalities to the offspring.