Abstract
There exist numerous experimental and epidemiological data indicating that malnutrition in early development may influence the risk of developing metabolic disorders in adult life, including type 2 diabetes mellitus (T2DM). Epidemiological evidence for such a relationship was mostly obtained in quasi-experimental studies (natural experiments) carried out on the populations of different countries. These studies revealed that exposure to famine in prenatal and/or early postnatal development is associated with increased risk of developing type 2 diabetes in adult life. Epigenetic regulation of gene activity is considered to be the main mechanism linking starvation in early life and increased risk of type 2 diabetes in adulthood. It is believed that exposure to famine during pregnancy may induce persistent epigenetic variations that are thought to have some adaptive value in the early postnatal development but that also lay grounds for metabolic disorders, including type 2 diabetes, in later life. The present review consolidates and discusses the data indicating the possibility of early developmental programming of type 2 diabetes obtained in the course of quasi-experimental studies.
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