Intrauterine malnutrition predisposes the offspring towards the development of type 2 diabetes and cardiovascular disease. To explain this association, the Developmental Origins of Health and Disease (DOHaD) hypothesis was introduced, meaning that subtle environmental changes during embryonic and fetal development can influence postnatal physiological functions. Different mechanisms, including epigenetics, are thought to be involved in this fetal programming, but the link between epigenetics and disease is missing. There is increasing evidence that ectopic lipid accumulation and/or lipotoxicity is induced by fetal programming. The aim of this review is to provide insights into the mechanisms underlying lipotoxicity through programming which contributes to the increase in hepatic and cardiac metabolic risk. This article is protected by copyright. All rights reserved.