摘要: The current epidemic of obesity and related cardiometabolic diseases is often linked to an obesogenic environment and sedentary behaviours. However, increasing evidence from human observational studies and experimental animal models suggests that alterations in the early-life nutritional environment can increase the susceptibility for the development of such disorders in adult life. This developmental programming falls under the “Developmental Origins of Health and Disease”(DOHaD) framework whereby adverse environmental impacts during the early-life period of developmental plasticity can result in adaptations that can have long-term adverse trade-offs in offspring for health outcomes across the lifecourse (Figure 2.1). 1, 2 The DOHAD model suggests that predictive adaptations are made in early life in response to environmental cues (eg malnutrition, resulting in the development of a “thrifty phenotype” 3) in order to maximise survival in the expected postnatal environment. However, when the interpretations of such prenatal cues