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Maternal epigenetics and fetal and neonatal growth.
Kitsiou-Tzeli, S, Tzetis, M
Current opinion in endocrinology, diabetes, and obesity. 2017;(1):43-46
Abstract
PURPOSE OF REVIEW The article provides an update on new insights of factors altering inherited maternal epigenome that ultimately affect fetal and neonatal growth. RECENT FINDINGS A number of new publications have identified mechanisms through which maternal nutrition, environmental exposures such as stress and toxic substances altering expression of imprinted genes during pregnancy can influence fetal and neonatal phenotype and susceptibility to disease development later in life. The possible causes of metabolic syndrome by in-utero epigenetic alterations of genes involved in energy metabolism (PPARγ and PPARα), microRNAs, arginine methyltransferases, lysine demethylases, and histone deacetylaces have been elucidated. Moreover associations between methylation of key genes (NRC31, HSD11β1/2, GFI1) involved in the hypothalamic-pituitary-adrenal axis have been identified. Alcohol exposure during pregnancy was found to alter methylation patterns of several imprinted genes (H19, SLC22A18, SLC6A3, DRD4). Finally alterations in vulnerable epigenetic marks of imprinted genes such as H19/IGF2, during early stages of embryonic development result in intrauterine growth restriction. SUMMARY All these investigations continue to provide new insights for improved clinical management of in-utero development.
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2.
Current thoughts on maternal nutrition and fetal programming of the metabolic syndrome.
Brenseke, B, Prater, MR, Bahamonde, J, Gutierrez, JC
Journal of pregnancy. 2013;:368461
Abstract
Chronic diseases such as type 2 diabetes and cardiovascular disease are the leading cause of death and disability worldwide. Although the metabolic syndrome has been defined in various ways, the ultimate importance of recognizing this combination of disorders is that it helps identify individuals at high risk for both type 2 diabetes and cardiovascular disease. Evidence from observational and experimental studies links adverse exposures in early life, particularly relating to nutrition, to chronic disease susceptibility in adulthood. Such studies provide the foundation and framework for the relatively new field of developmental origins of health and disease (DOHaD). Although great strides have been made in identifying the putative concepts and mechanisms relating specific exposures in early life to the risk of developing chronic diseases in adulthood, a complete picture remains obscure. To date, the main focus of the field has been on perinatal undernutrition and specific nutrient deficiencies; however, the current global health crisis of overweight and obesity demands that perinatal overnutrition and specific nutrient excesses be examined. This paper assembles current thoughts on the concepts and mechanisms behind the DOHaD as they relate to maternal nutrition, and highlights specific contributions made by macro- and micronutrients.
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3.
Programming of body composition by early growth and nutrition.
Wells, JC, Chomtho, S, Fewtrell, MS
The Proceedings of the Nutrition Society. 2007;(3):423-34
Abstract
There is now compelling evidence that growth patterns in early life are associated with risk of the metabolic syndrome in adulthood, although the relative importance of prenatal v. postnatal growth for such associations remains controversial. Body composition may play a key role in the 'programming' of such diseases, through itself being programmed by early growth, and perhaps also by being a mediator of the programming process. Early studies reporting positive associations between birth weight and adult BMI suggested a tendency for large babies to become obese adults. Such findings appeared contradictory to the many studies linking low birth weight with increased risk of the metabolic syndrome. Recent studies now indicate that birth weight is strongly predictive of later lean mass, and has a much weaker association with later fatness. Studies that link low birth weight with a more central adipose distribution in later life remain controversial, and require confirmation using more sophisticated methodologies. Findings for infant growth rate appear population-specific, with infant weight gain predicting subsequent lean mass in developing countries, but predicting subsequent fat mass and obesity in industrialised populations. Further studies are required on this issue, to ensure that appropriate public health policies are recommended for countries across the range of economic development. Although the links between early growth and later disease risk implicate early-life nutrition, either in utero or during infancy, few prospective studies have explored the influence of early diet on later body composition. Many studies have associated breast-feeding with a reduced prevalence of obesity categorised by BMI; however, the few studies directly evaluating childhood fatness provide little support for this hypothesis. Recent advances in the ability to measure body composition during the infant period offer a major opportunity to improve the understanding of the nutritional programming of body composition and its contribution, or lack thereof, to subsequent disease risk.
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4.
Tracing the origins of "fetal origins" of adult diseases: programming by oxidative stress?
Luo, ZC, Fraser, WD, Julien, P, Deal, CL, Audibert, F, Smith, GN, Xiong, X, Walker, M
Medical hypotheses. 2006;(1):38-44
Abstract
Too small size at birth (due to poor fetal growth and/or preterm delivery) has been associated with substantially elevated risks of the metabolic syndrome (dislipidemia, insulin resistance, hypertension), type 2 diabetes and cardiovascular disease in adulthood. The mechanisms of such "fetal origins" or "programming" of disease phenomenon remain unresolved. Too large size at birth seems also associated with an increased risk. Many known or suspected causes of or conditions associated with adverse (poor or excessive) fetal growth or preterm birth have been associated with oxidative stress. Plausibly, oxidative stress may be a common link underlying the superficial "programming" associations between adverse fetal growth or preterm birth and elevated risks of certain chronic diseases. The mechanisms of oxidative stress programming may be through directly modulating gene expression or indirectly through the effects of certain oxidized molecules. Experimental investigations have well demonstrated the role of redox balance in modulating gene expression, and recent studies indicate that both the insulin functional axis and blood pressure could be sensitive targets to oxidative stress programming. Adverse programming may occur without affecting fetal growth, but more frequently among low birth weight infants merely because they more frequently experienced known or unknown conditions with oxidative insults. As oxidative stress levels are easily modifiable during pregnancy and early postnatal periods (which are plausible critical windows), the hypothesis, if proved valid, will suggest new measures that could be very helpful on fighting the increasing epidemic of the metabolic syndrome, type 2 diabetes and cardiovascular disease. Currently, there are several ongoing large randomized trials of antioxidant supplementation to counter oxidative stress during pregnancy for the prevention of preeclampsia. It would be invaluable if long-term follow-ups of infants born to women in such trials could be realized to test the oxidative stress programming hypothesis in such experimental trial settings.
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5.
[Fetus and magnesium].
Takaya, J, Kaneko, K
Clinical calcium. 2005;(11):105-10
Abstract
Chronic magnesium deficiency in pregnant women is frequently seen because of inadequate or low intake of magnesium. Magnesium deficiency during pregnancy can induce not only maternal and fetal nutritional problem, but also pediatric consequences that might last throughout life. Many epidemiological studies have disclosed that restricted fetal growth, i.e., intrauterine growth retardation (IUGR) is associated with an increased risk of insulin resistance in adult life. We previously postulated that intracellular magnesium of cord blood platelets is lower in the small for gestational age than in the appropriate for gestational age group, suggesting chronic intrauterine magnesium deficiency may result in IUGR. Taken together, chronic intrauterine magnesium deficiency in the fetus may lead to or program the insulin resistance after birth. Prospective study whether the children born with magnesium induced IUGR are at high-risk for metabolic syndrome in childhood or adulthood is currently undertaken.