Epidemiological evidence suggests that in utero as well as early postnatal life exposure to an imbalanced nutrition are both related to a greater propensity to become obese in later life. Rodent and sheep models of metabolic programming of obesity by early life nutrition include maternal low and high dietary protein and energy or food intake as well as high fat diets. Maternal nutritional imbalance during pregnancy and/or lactation programs energy expenditure, food intake and physical activity in the offspring. Underlying mechanisms of altered energy balance in programmed offspring are associated with disturbances of ontogeny of hypothalamic feeding circuits, leptin and glucocorticoid action which have long-lasting effects on food intake, energy expenditure and fat tissue metabolism.