Maternal Nutrition and Developmental Programming of Obesity

Author(s):  
Fátima Martel ◽  
Elisa Keating
Epigenetics ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. 1200-1210 ◽  
Author(s):  
Elena Ivanova ◽  
Jian-Hua Chen ◽  
Anne Segonds-Pichon ◽  
Susan E. Ozanne ◽  
Gavin Kelsey

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 894 ◽  
Author(s):  
Hsu ◽  
Tain

Maternal nutrition plays a decisive role in developmental programming of many non-communicable diseases (NCDs). A variety of nutritional insults during gestation can cause programming and contribute to the development of adult-onset diseases. Nutritional interventions during pregnancy may serve as reprogramming strategies to reverse programming processes and prevent NCDs. In this review, firstly we summarize epidemiological evidence for nutritional programming of human disease. It will also discuss evidence from animal models, for the common mechanisms underlying nutritional programming, and potential nutritional interventions used as reprogramming strategies.


2011 ◽  
Vol 94 (suppl_6) ◽  
pp. 1846S-1852S ◽  
Author(s):  
Claude Remacle ◽  
Florence Bieswal ◽  
Vanesa Bol ◽  
Brigitte Reusens

2014 ◽  
Vol 54 (9) ◽  
pp. 1465 ◽  
Author(s):  
P. R. Kenyon ◽  
R. A. Corner-Thomas ◽  
S. W. Peterson ◽  
S. J. Pain ◽  
H. T. Blair

In sheep, maternal nutrition can affect the offspring’s milk production at its first lactation and the grand-offspring’s liveweight to weaning. However, this apparent developmental programming effect on milk production and grand-offspring liveweight has not persisted. Therefore, the aim of the present study was to determine if nutrition of the programmed ewe in mid- to late pregnancy affected this response. Developmentally programmed ewes (G1) that had been born from dams (G0) offered submaintenance, maintenance or ad libitum feeding levels from Day 21 to Day 50 of pregnancy and then either pregnancy maintenance or ad libitum to Day 140 were used for this study. These ewes were offered one of two pastoral-based pregnancy nutritional treatments (controlled vs unrestricted) from Day 76 of pregnancy until lambing. Pre- and post-herbage masses of the unrestricted treatment (2181 ± 47.6 and 1431 ± 24.6 kg DM/ha, respectively), were greater (P < 0.05) than the controlled treatment (1164 ± 31.6 and 819 ± 16.0 kg DM/ha, respectively). At Day 71 of pregnancy, there were no differences (P > 0.05) in G1 liveweight (70.2 ± 0.8 vs 70.3 ± 0.8 kg for controlled and unrestricted feeding, respectively), or body condition scores (2.5 ± 0.06 vs 2.5 ± 0.05) between pregnancy nutritional treatments. In late pregnancy, unrestricted G1 ewes were heavier (P < 0.05, 97.4 ± 1.0 vs 86.8 ± 1.0 kg) and had greater (P < 0.05) body condition scores (3.4 ± 0.06 vs 2.5 ± 0.06) and back-fat depths (8.0 ± 0.3 vs 5.9 ± 0.03 mm) than controlled nutritional treatment ewes. There were no interactions (P > 0.05) between grand-dam feeding levels and ewe nutritional treatment on lamb (G2) liveweights at birth or in lactation. This indicates that under the conditions of the present study, nutrition of the G1 ewe did not affect the expression of the developmental programming effect. Further studies might be warranted to determine the causes of this inconsistency in grand-offspring liveweight. Nutrition of the G1 ewe had a minor effect (P < 0.05) on G2 lamb birthweight and liveweight in early lactation but not (P > 0.05) in late lactation or on lamb survival. These findings indicate there is no little to no benefit to the lamb until weaning from offering ewes pre- and post-grazing masses above ~1200 and 800 kg DM/ha, respectively, in mid- to late pregnancy.


2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.


2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 121-121
Author(s):  
Allison M Meyer

Abstract Mineral nutrition during pregnancy has long been known to impact fetal growth and development. This is evidenced by a multitude of mineral deficiency-related causes for embryonic loss, abortion, stillbirth, or neonatal death, including poor or inappropriate fetal development that can be either reversible or irreversible postnatally. Both macro and trace mineral needs of the dam are known to increase with the fetal growth of advancing gestation due to greater metabolic stress and demand, as well as tissue development and deposition in the fetus. Fetal deposition of many trace minerals is especially important for neonatal use while consuming milk with low mineral concentrations and facing a multitude of immune challenges. In the last 2 decades, many laboratories have focused on “developmental programming,” or the effects of maternal nutrition on fetal and neonatal development and ultimately long-term health and productivity of livestock. Despite this, the role of macro and trace minerals in short-and long-term consequences of developmental programming is still unclear for many minerals and species. Taken together, research in ruminants and swine demonstrate that mineral intake and source during pregnancy can have a large effect on fetal growth and development that lasts into the neonatal and pre-weaning periods. Some studies suggest that supra-nutritional mineral intake may have a positive benefit during gestation or neonatal periods. Moreover, some data suggest that mineral requirements may be greater than currently thought to accommodate the rapid fetal growth and preparation for lactation that occurs during late gestation. Continued research is necessary to determine mineral requirements of livestock during pregnancy, especially when considering their long-reaching subsequent effects on offspring. Additionally, increased understanding of perinatal transfer of trace minerals can aid in our management of pregnant dams and their offspring.


Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1917 ◽  
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain

Hypertension is a growing global epidemic. Developmental programming resulting in hypertension can begin in early life. Maternal nutrition status has important implications as a double-edged sword in the developmental programming of hypertension. Imbalanced maternal nutrition causes offspring’s hypertension, while specific nutritional interventions during pregnancy and lactation may serve as reprogramming strategies to reverse programming processes and prevent the development of hypertension. In this review, we first summarize the human and animal data supporting the link between maternal nutrition and developmental programming of hypertension. This review also presents common mechanisms underlying nutritional programming-induced hypertension. This will be followed by studies documenting nutritional interventions as reprogramming strategies to protect against hypertension from developmental origins. The identification of ideal nutritional interventions for the prevention of hypertension development that begins early in life will have a lifelong impact, with profound savings in the global burden of hypertension.


2013 ◽  
Vol 4 (5) ◽  
pp. 328-337 ◽  
Author(s):  
D. A. Giussani ◽  
S. T. Davidge

It is now recognized that the quality of the fetal environment during early development is important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. However, in contrast to the extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only recently becoming delineated and established. This review discusses the increasing body of evidence supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the identification of plausible mechanisms and the implementation of maternal and early life interventions to protect against adverse programming.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wellison J. S. Diniz ◽  
Matthew S. Crouse ◽  
Robert A. Cushman ◽  
Kyle J. McLean ◽  
Joel S. Caton ◽  
...  

AbstractThe molecular basis underlying fetal programming in response to maternal nutrition remains unclear. Herein, we investigated the regulatory relationships between genes in fetal cerebrum, liver, and muscle tissues to shed light on the putative mechanisms that underlie the effects of early maternal nutrient restriction on bovine developmental programming. To this end, cerebrum, liver, and muscle gene expression were measured with RNA-Seq in 14 fetuses collected on day 50 of gestation from dams fed a diet initiated at breeding to either achieve 60% (RES, n = 7) or 100% (CON, n = 7) of energy requirements. To build a tissue-to-tissue gene network, we prioritized tissue-specific genes, transcription factors, and differentially expressed genes. Furthermore, we built condition-specific networks to identify differentially co-expressed or connected genes. Nutrient restriction led to differential tissue regulation between the treatments. Myogenic factors differentially regulated by ZBTB33 and ZNF131 may negatively affect myogenesis. Additionally, nutrient-sensing pathways, such as mTOR and PI3K/Akt, were affected by gene expression changes in response to nutrient restriction. By unveiling the network properties, we identified major regulators driving gene expression. However, further research is still needed to determine the impact of early maternal nutrition and strategic supplementation on pre- and post-natal performance.


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