Abstract
Nutritional changes during developmental windows are of particular concern in offspring metabolic disease. Questions are emerging concerning the role of maternal weight changes before conception, particularly for weight loss, in the development of diet-related disorders. Understanding the physiological pathways affected by the maternal trajectories in the offspring is therefore essential, but a broad overview is still lacking. We recently reported both metabolic and behavioral negative outcomes in offspring born to obese or weight-loss mothers and fed a control of high-fat diet, suggesting long-term modeling of metabolic pathways needing to be further characterized. Using non-targeted LC–HRMS, we investigated the impact of maternal and post-weaning metabolic status on the adult male offspring’s metabolome in three tissues involved in energy homeostasis: liver, hypothalamus and olfactory bulb. We showed that post-weaning diet interfered with the abundance of several metabolites, including 1,5-anhydroglucitol, saccharopine and β-hydroxybutyrate, differential in the three tissues. Moreover, maternal diet had a unique impact on the abundance of two metabolites in the liver. Particularly, anserine abundance, lowered by maternal obesity, was normalized by a preconceptional weight loss, whatever the post-weaning diet. This study is the first to identify a programming long-term effect of maternal preconception obesity on the offspring metabolome.
Highlights
In 2016, the worldwide prevalence of obesity in adult women was 15% [1]
Its morphology and functions are altered in utero in the context of maternal obesity and/or a high-fat diet (HFD), which contributes to the development of non-alcoholic fatty liver disease (NAFLD) in adulthood [11,12,13]
We propose that a hepatic defect in HFD-fed males may affect the production of 1,5-AG, decreasing its concentration in the blood delivered to other tissues, as observed here for HYP and whole olfactory bulb (WOB)
Summary
In 2016, the worldwide prevalence of obesity in adult women was 15% [1]. Maternal obesity is a risk factor for metabolic and obstetric complications during pregnancy [2], and for fetal outcomes because it is associated with a higher risk of the fetus being large or small for gestational age [3,4,5].This affects fetal organogenesis and, organ function after birth [6] and seems largely associatedNutrients 2020, 12, 1572; doi:10.3390/nu12061572 www.mdpi.com/journal/nutrientsNutrients 2020, 12, 1572 with the offspring’s long-term obesity risk, as stated by the concept of the developmental origins of health and disease (DOHaD) [7].Given the many risks to both mother and child, overweight women are advised to lose weight before conception [8], little is known about the consequences of a nutritional intervention, for fetal and tissue development or their long-term effects [9]. Maternal obesity is a risk factor for metabolic and obstetric complications during pregnancy [2], and for fetal outcomes because it is associated with a higher risk of the fetus being large or small for gestational age [3,4,5]. This affects fetal organogenesis and, organ function after birth [6] and seems largely associated. The consequences of a preconceptional maternal weight loss on brain metabolism and associated functions of the progeny remain poorly investigated [22,23]
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