Abstract
Despite constant research and public policy efforts, the obesity epidemic continues to be a major public health threat, and new approaches are urgently needed. It has been shown that nutrient imbalance in early life, from conception to infancy, influences later obesity risk, suggesting that obesity could result from “developmental programming”. In this review, we evaluate the possibility that early postnatal nutrition programs obesity risk via epigenetic mechanisms, especially DNA methylation, focusing on four main topics: (1) the dynamics of epigenetic processes in key metabolic organs during the early postnatal period; (2) the epigenetic effects of alterations in early postnatal nutrition in animal models or breastfeeding in humans; (3) current limitations and remaining outstanding questions in the field of epigenetic programming; (4) candidate pathways by which early postnatal nutrition could epigenetically program adult body weight set point. A particular focus will be given to the potential roles of breast milk fatty acids, neonatal metabolic and hormonal milieu, and gut microbiota. Understanding the mechanisms by which early postnatal nutrition can promote lifelong metabolic modifications is essential to design adequate recommendations and interventions to “de-program” the obesity epidemic.
Highlights
Obesity is a major risk factor for many serious chronic pathologies, including type 2 diabetes, cardiovascular diseases, and cancers [1]
We evaluate the possibility that early postnatal nutrition programs obesity risk via epigenetic mechanisms
We review animal models of obesity programming triggered by nutritional alteration in the lactation-suckling period and summarize the evidence of epigenetic remodeling observed in these models
Summary
Obesity is a major risk factor for many serious chronic pathologies, including type 2 diabetes, cardiovascular diseases, and cancers [1]. Epidemiologic and animal studies have shown that early postnatal nutrition alone, independently of the in utero milieu, can influence obesity risk. Animal studies have confirmed that altered nutrition in mothers or pups during lactation-suckling is sufficient to determine long-term adiposity in offspring [13,14,15,16]. Understanding the mechanisms by which early postnatal nutrition influences the adult body weight “set point” would offer the opportunity to design targeted recommendations and interventions for long-term benefits. We evaluate the possibility that early postnatal nutrition programs obesity risk via epigenetic mechanisms. We discuss the role of breast milk fatty acids, neonatal metabolic and hormonal milieu, and gut microbiota in the epigenetic programming of obesity. Our long-term goal is to define the precise mediators and pathways by which postnatal nutrition can promote lifelong metabolic (mal)adaptations in order to design potential diagnostic and therapeutic tools that could be used to “de-program” this vicious circle of obesity propagation
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