This article reviews the evidence for fetal and early origins of type 2 diabetes, insulin resistance, dyslipidaemia and obesity. Particular emphasis is given to the role of adipose tissue in catch-up growth and long-term metabolic complications following restricted fetal growth. To date, several pathways have been proposed to explain the development of insulin resistance following restricted fetal growth, but no precise mechanisms have been demonstrated. It appears that early postnatal growth may also be a critical step.