Long-term metabolic risk among children born premature or small for gestational age

Abstract

Accumulating evidence suggests that both the intrauterine environment and growth during early life can influence the development of chronic noncommunicable diseases, such as type 2 diabetes mellitus and cardiovascular disease, in adulthood. Here, we review the available human data supporting increased metabolic risk among children born premature or small for gestational age; the adrenal and pubertal modifications that contribute to this risk; metabolic changes that occur during adolescence and early adulthood; and approaches to potentially modify or decrease risk of metabolic disease. The risks associated with delivery at term or preterm are compared for each period of life. Knowledge of these associations is fundamental for the paediatric community to develop preventive strategies early during postnatal life.

Prenatal programming of later performance in dairy cattle

“…The high insulin sensitivity in small infants is often associated with an accelerated postnatal body growth, referred to as 'catch-up growth' (Gafni and Baron, 2000;Ibáñez et al, 2006), but also results in early obesity and peripheral insulin resistance (Soto et al, 2003;Ibáñez et al, 2006). Hence, IUGR has been linked with an increased risk of diabetes during later life, but also other health problems like elevated blood pressure, cardiovascular disease and even reproductive disorders (Ibáñez et al, 1998;Roseboom et al, 2001;Ibánez et al, 2008;Mericq et al, 2017). The aforementioned findings have led to the 'Developmental Origin of Health and Disease (DOHaD)' hypothesis (Hales et al, 1991), stating that besides genotype, the prenatal and early postnatal environment influences the development of chronic diseases.…”

Epigenetic Mechanisms of Transmission of Metabolic Disease across Generations

“…Independent of nutritional factors, low birth weight itself increases the risk of metabolic disease in adult life (Barker, 2000; Mericq et al, 2016). David Barker was the first to identify relationships between birth weight and the development of cardiovascular and other metabolic disease during adult life (Barker, 2000).…”

“…In a recent review, Mericq summarized the extensive body of literature supporting the association between children born small for gestational age or premature and the subsequent development of metabolic disease (i.e. higher glucose levels, T2D, cardiovascular disease) (Mericq et al, 2016). These associations are further magnified when low birth weight individuals experience postnatal “catch-up growth” (Dulloo, 2009).…”

Towards a simple marker of hepato‐visceral adiposity and insulin resistance: The Z‐score change from weight‐at‐birth to BMI‐in‐childhood

“…Early treatment of insulin resistance and hepato‐visceral fat excess requires an early diagnosis of these abnormalities, and such early diagnosis is nowadays cumbersome and costly, since it requires dynamic blood testing and magnetic resonance imaging (MRI). Insulin resistance and hepato‐visceral adiposity are thought to contribute to advancing milestones such as adrenarche/pubarche and puberty/menarche into a younger age range . In turn, an earlier timing of these milestones relates often to a mismatch between prenatal and postnatal weight gain, which can readily be estimated by calculating the Z‐score change from weight at birth to body mass index (BMI) in childhood .…”

“…Insulin resistance and hepato-visceral adiposity are thought to contribute to advancing milestones such as adrenarche/pubarche and puberty/ menarche into a younger age range. 1,2 In turn, an earlier timing of these milestones relates often to a mismatch between prenatal and postnatal weight gain, 3,4 which can readily be estimated by calculating the Z-score change from weight at birth to body mass index (BMI) in childhood. 1 We posited that this calculation may also serve as a proxy of insulin resistance and hepato-visceral adiposity in prepubertal children.…”