Overnutrition in the early postnatal period influences lifetime metabolic risk: Evidence for impact on pancreatic β‐cell mass and function

Overconsumption of energy‐rich foods that disrupt caloric balance is a fundamental cause of overweight, obesity and diabetes. Dysglycemia and the resulting cardiovascular disease cause substantial morbidity and mortality worldwide, as well as high societal cost. The prevalence of obesity in childhood and adolescence is increasing, leading to younger diabetes diagnosis, and higher severity of microvascular and macrovascular complications. An important goal is to identify early life conditions that increase future metabolic risk, toward the goal of preventing diabetes and cardiovascular disease. An ample body of evidence implicates prenatal and postnatal childhood growth trajectories in the programming of adult metabolic disease. Human epidemiological data show that accelerated childhood growth increases risk of type 2 diabetes in adulthood. Type 2 diabetes results from the combination of insulin resistance and pancreatic β‐cell failure, but specific mechanisms by which accelerated postnatal growth impact one or both of these processes remain uncertain. This review explores the metabolic impact of overnutrition during postnatal life in humans and in rodent models, with specific attention to the connection between accelerated childhood growth and future adiposity, insulin resistance, β‐cell mass and β‐cell dysfunction. With improved knowledge in this area, we might one day be able to modulate nutrition and growth in the critical postnatal window to maximize lifelong metabolic health. Diabetes causes substantial morbidity and mortality worldwide, as well as high societal cost. Risk of metabolic disease in adulthood increases in people with accelerated childhood growth trajectory. This review explores the metabolic impact of postnatal overnutrition in humans and in rodent models, with specific attention to the connection between accelerated childhood growth and future adiposity, insulin resistance, β‐cell mass and β‐cell dysfunction.