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Review
. 2019 Sep;20(6):428-437.
doi: 10.2174/1389202920666191118092852.

Epigenetic Programming of Adipose Tissue in the Progeny of Obese Dams

Simon Lecoutre  1   2 , Kelvin H M Kwok  3 , Paul Petrus  2 , Mélanie Lambert  2 , Christophe Breton  1
Affiliations
Review

Epigenetic Programming of Adipose Tissue in the Progeny of Obese Dams

Simon Lecoutre et al. Curr Genomics. 2019 Sep.

Abstract

According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and the resulting accelerated growth in neonates predispose offspring to obesity and associated metabolic diseases that may persist across generations. In this context, the adipose tissue has emerged as an important player due to its involvement in metabolic health, and its high potential for plasticity and adaptation to environmental cues. Recent years have seen a growing interest in how maternal obesity induces long-lasting adipose tissue remodeling in offspring and how these modifications could be transmitted to subsequent generations in an inter- or transgenerational manner. In particular, epigenetic mechanisms are thought to be key players in the developmental programming of adipose tissue, which may partially mediate parts of the transgenerational inheritance of obesity. This review presents data supporting the role of maternal obesity in the developmental programming of adipose tissue through epigenetic mechanisms. Inter- and transgenerational effects on adipose tissue expansion are also discussed in this review.

Keywords: Perinatal period; developmental origin of health and disease; epigenome; fat expansion; gene expression; maternal obesity.

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Figures

Fig. (1)
Fig. (1)
Inter- and transgenerational inheritance of adipose tissue dysfunction in offspring from obese mothers. Maternal obesity implies that three generations are exposed to the nutritional environment: the pregnant mother (F0), the fetus (F1) and the germline of the fetus (the future F2). Altered nutritional and hormonal microenvironment induced by maternal obesity (F0) may alter chromatin remodeling during adipose tissue development in the prenatal or postnatal period (F1), as can the germline of the fetus (the future F2). These epigenetic remodeling leads to the deregulation of many genes essential for the adipocyte function. Once the epigenomic changes are established during the perinatal period, they might persist into adulthood as an epigenetic memory, resulting in obesity predisposition in adulthood. These are considered to be parental effects, leading to intergenerational epigenetic inheritance. A transgenerational effect refers to that found only in the F3 generation, which is not exposed to direct malnutrition as experienced by F0-F2 generations.
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