Pancreatic insulin secretion is plastic, adapting in response to changing demand for insulin. In most individuals, insulin secretion increases in response to falling insulin sensitivity, and is able to maintain insulin action. This plasticity of insulin secretion can occur through changes in β-cell mass and β-cell function, and type 2 diabetes only occurs if these processes fail. Poor growth before birth occurs in 6-12% of pregnancies in developed countries, and increases the risk of adult-onset metabolic diseases, including type 2 diabetes. Insulin sensitivity is consistently lower in adult humans who were growth-restricted before birth (IUGR), compared to those who were appropriately growth at birth. A number of studies in humans have shown that insulin secretion fails to increase sufficiently to maintain insulin action and glycaemic control in the face of insulin resistance in the IUGR population. Our studies in the IUGR sheep suggest that failure of β-cell function is the main cause of this inadequate insulin secretion after IUGR. Most recently, we have confirmed that restricted placental growth, a major cause of IUGR in humans, impairs postnatal capacity to control glucose when challenged by mild hyperglycaemia, providing the first direct evidence that IUGR impairs plasticity of insulin secretion.