Chapter 11 - Early life nutrition and its effect on the development of obesity and type-2 diabetes

Abstract

The rising epidemics of obesity and type 2 diabetes (T2DM) represent a major global health burden with the rising incidence of the disorders in childhood and adolescence of particular concern. Further, rapid urbanization in developing countries has driven changes in lifestyle and dietary exposures, and these transitions are accompanied by increases in risk factors for obesity and non-communicable diseases including T2DM. In this context, extensive evidence from human cohorts and experimental animal models has established a clear relationship between the early life nutritional environment and later offspring predisposition toward obesity and a range of metabolic disorders. This process, preferentially termed “developmental programming,” has shown that maternal, and more recently paternal, nutrition plays a key role in the programming of disease risk in offspring. Moreover, these effects can be passed on to future generations via either the maternal or paternal lineage. Although the mechanisms remain poorly defined, they likely involve epigenetic processes as epigenetic dysregulation underpins several components of obesity and T2DM risk, including altered appetite regulation and insulin signaling in parallel to changes in adipogenesis and inflammatory processes. Increasing our understanding of the potential mechanisms through which an altered nutritional environment in early life can result in lifelong changes in metabolic processes is essential for designing adequate recommendations and interventions to break the cycle of disease underpinning the current epidemics of T2DM and obesity. This review will cover current human evidence and those derived from experimental models, mechanisms for programming obesity and T2DM, and potential strategies for intervention during early life development.