Foetal developmental origins of adult onset non-insulin dependent diabetes mellitus

Abstract There is a global non-insulin dependent diabetes mellitus epidemic, and through understanding the foetal origins of the disease it may become possible to impact the development of the disease. During pregnancy a foetus is entirely dependent on nutrients supplied by the mother via the placenta, meaning alterations to the composition or quantity of maternal nutrition can lead to infants being born with low birth weights. Low birth weight is classified as a weight at birth of ≤ 2.5 kg by the World Health Organisation. In 1990 Dr. David Barker published the “foetal origins of adult disease” hypothesis in order to explain the observed epidemiological relationship between birth-weight and future disease development. It is now understood that alterations to gene expression occurring during foetal development, can then go on to increase the risk developing chronic non-communicable diseases, such as noninsulin dependent diabetes mellitus (NIDDM) in adulthood. However, the exact mechanisms through which this takes place remains unclear. The events during development which result in diminished foetal growth are multifactorial. A foetus’s maximal growth potential is determined genetically, however maternal nutrition both pre and post conception is capable of influencing growth trajectory. This review will examine the existing body of evidence regarding the role of adaptive changes occurring during foetal development in relation to the subsequent development of NIDDM in adulthood. As well as considering the potential mechanisms through which these events could be mediated.