Early Life Nutrition and its Effect on the Development of Type-2 Diabetes

Abstract

Diabetes is one of the most common metabolic disorders in the world and the prevalence of diabetes in adults has been increasing in the last decades. In particular, urbanization in developing countries has driven dramatic changes in lifestyle and these rapid transitions are accompanied by increases in risk factors for noncommunicable diseases including type-2 diabetes (T2DM). Although the changes in prevalence result in part from increased rates of obesity in those individuals with a genetic predisposition to T2DM, the recent increases in T2DM rates suggests that other environmental factors are key contributors to disease susceptibility. In this context, extensive evidence from human cohorts and experimental animal models has now clearly established a link between the early life nutritional environment and later risk in offspring for a range of cardiometabolic disorders. This process, preferentially called “developmental programming,” has shown that maternal, and more recently paternal nutrition, plays a key role in metabolic programming of the offspring. Although the mechanisms remain poorly defined, they likely involve epigenetics, as epigenetic dysregulation is associated with several components of T2DM risk, including altered feeding behavior and insulin secretion and action and may also contribute to transgenerational transmission of T2DM risk. This review will cover the current human and experimental evidence, potential mechanisms for programming of T2DM, and interventions strategies during the early period of developmental plasticity.