Early growth and postprandial glucose, insulin, lipid and inflammatory responses in adulthood

Purpose of review Epidemiological findings suggest that prenatal and postnatal growth is associated with later health outcomes including cardiovascular disease and type 2 diabetes. It has been suggested that these associations are mediated through classical risk factors, for example dyslipidemia. Despite extensive epidemiological investigations, only limited data are available on the long-term influences of early growth on postprandial responses, although postprandial levels of many risk factors have been proposed to be more important than fasting levels in disease process. This review focuses on recent studies evaluating the effect of early growth on postprandial responses. Recent findings Current evidence from postprandial studies shows that individuals who were small at birth or grew slowly during infancy have elevated postprandial insulin and triglyceride responses. However, early growth does not seem to affect postprandial inflammatory markers. It is likely that both liver programming and abnormalities in insulin-sensitive tissues play key roles in explaining these elevated responses. Summary Recent studies suggest that slow growth during early life has an adverse effect on postprandial metabolism, and predicts higher insulin and triglyceride responses. These elevated postprandial responses might be one underlying mechanism explaining the increased risk of cardiovascular disease and type 2 diabetes associated with nonoptimal early growth.