Abstract
Based on the concept of Developmental Origin of Health and Disease, both human and animal studies have demonstrated a close link between nutrient supply perturbations in the fetus or neonate (i.e., maternal undernutrition, obesity, gestational diabetes and/or rapid catch-up growth) and increased risk of adult-onset obesity. Indeed, the adipose tissue has been recognized as a key target of developmental programming in a sex-and depot-specific manner. Despite different developmental time windows, similar mechanisms of adipose tissue programming have been described in rodents and in bigger mammals (sheep, primates). Maternal nutritional manipulations reprogram offspring's adipose tissue resulting in series of alterations: enhanced adipogenesis and lipogenesis, impaired sympathetic activity with reduced noradrenergic innervations and thermogenesis as well as low-grade inflammation. These changes affect adipose tissue development, distribution and composition predisposing offspring to fat accumulation. Modifications of hormonal tissue sensitivity (i.e., leptin, insulin, glucocorticoids) and/or epigenetic mechanisms leading to persistent changes in gene expression may account for long-lasting programming across generations.
Highlights
Unité Environnement Périnatal et Santé, UPRES EA 4489, Equipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, Université de Lille, Villeneuve d’Ascq, France
Based on the concept of Developmental Origin of Health and Disease, both human and animal studies have demonstrated a close link between nutrient supply perturbations in the fetus or neonate and increased risk of adult-onset obesity
Modifications of hormonal tissue sensitivity and/or epigenetic mechanisms leading to persistent changes in gene expression may account for long-lasting programming across generations
Summary
Unité Environnement Périnatal et Santé, UPRES EA 4489, Equipe Malnutrition Maternelle et Programmation des Maladies Métaboliques, Université de Lille, Villeneuve d’Ascq, France. Similar outcomes (i.e., neonatal hyperinsulinemia, hypertrophied adipocytes, exacerbated lipogenesis and obesity later in life) were associated with artificially reared rat pups fed a formula high in carbohydrate-derived energy These findings highlight the importance of modified perinatal glucose and/or insulin levels in programming events (Srinivasan et al, 2008). Elevated pro-inflammatory markers in WAT, possibly originating from immune cell infiltration were reported in fetus of obese mice fed a cafeteria diet before mating and throughout gestation (Murabayashi et al, 2013) This phenomenon occurred at an early stage of WAT development in line with increased storage of TG in prenatally undernourished adult sheep (Sharkey et al, 2009) and rat offspring following uteroplacental insufficiency (Joss-Moore et al, 2010). It remains to determine whether inflammatory changes are cause or consequence of fat accumulation
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