Nutritional signals of maternal origin include metabolites such as glucose and fatty acids, and hormones that reflect body composition and the size of short term and long term energy stores, such as leptin (released by body fat) and insulin. These blood borne factors are likely to influence metabolic outcomes in offspring in later life, with deleterious outcomes likely from the opposite extremes of maternal nutrition. Accordingly, malnutrition in utero which may result from low maternal calorie intake or inadequate dietary protein can give rise to intrauterine growth restriction (IUGR) and result in metabolic characteristics in the offspring that are not well suited to a postnatal life where calories are plentiful. Such outcomes can increase the risk of obesity and insulin resistance in later life in the offspring. Alternatively, maternal overweight and obesity, which are often accompanied by chronic or gestational diabetes (high blood glucose levels), will also result in high blood leptin levels, and can lead to elevated fetal insulin levels that promote growth and adiposity in the offspring. In early post-natal life, the influence of maternal body composition can continue in the form of leptin from suckled milk, which can be absorbed across the neonatal gut. The emerging role of leptin in the development of energy balance circuits in the brain could make this another determinant of the differential growth rates seen in breast and formula-fed human infants. It appears increasingly likely that maternal obesity is predisposing offspring to over-consumption of calories and increased body fatness in later life. As such, this represents an important non-genetic route of transmission across generations.