A large body of evidence supports the hypothesis that the risk of developing chronic diseases including type 2 diabetes (T2D) in adulthood is related to body size at birth. Birth weight may reflect fetal adaptation to an adverse intrauterine environment due to both genetic and environmental factors. Epidemiologic studies, primarily from prospective cohorts, have consistently shown that birth weight in the 2,500-4,000 g range is inversely associated with T2D risk in adulthood, while increased risk has been found at both extremes of low (< 2,500g) and high (> 4,000g) birth weight. The association between birth weight and risk of T2D can be modified by postnatal growth. Recent evidence appears to support that low birth weight may be related to rapid postnatal weight gain, which has been associated with increased risk for central obesity and T2D in adult life. Several mechanisms have been proposed to explain the robust association between birth weight and T2D. The "fetal origins hypothesis" remains the most popular one and has been revised based on recent evidence. This review aims to summarize both epidemiological and experimental observations relating birth weight and rapid postnatal weight gain to T2D risk in adulthood. This article will also highlight recent evidence on the mechanisms of fetal programming of diabetes due to maternal and fetal genetic factors as well as fetal epigenetic changes.
|Original language||English (US)|
|Title of host publication||Handbook of Anthropometry|
|Subtitle of host publication||Physical Measures of Human Form in Health and Disease|
|Publisher||Springer New York|
|Number of pages||18|
|State||Published - Jan 1 2012|
ASJC Scopus subject areas