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Fetal Programming of Type 2 Diabetes

Hales and Barker (1) caused a paradigm shift in our thinking about diabetes prevention when they demonstrated that low birth weight (due to growth retardation) predicted type 2 diabetes (the “thrifty phenotype” or “fetal origins” hypothesis). On the other hand, larger babies of diabetic mothers are also at higher risk of diabetes, apart from their genetic susceptibility (“fuel mediated teratogenesis”) (2,3). A concept evolved that the intrauterine experiences mold the fetal systems (“programming”) and influence future health (4). If the postnatal experiences are at variance with the intrauterine ones, the programmed fetus is susceptible to disease (5). For example, low birth weight babies who put on excess weight in later life are at a higher risk of type 2 diabetes than those who continue to be low weight (6). In the programming hypothesis, the focus is on the role of intrauterine environment and on gene-environment interaction rather than the differences in gene structure, which are the basis of conventional genetics. Genes are clearly important, and their role in intrauterine development and risk of diabetes was highlighted by Hattersley and Tooke (the “fetal insulin hypothesis”) (7). The most exciting thought in fetal programming is that intrauterine environment may modify gene expression permanently. A heritable change in gene expression without a change in DNA sequence is called “epigenetic” (8), a term first used by Waddington in developmental biology. Epigenetic changes alter gene function and can be silencing …