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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.
Impact of maternal nutritional status before and during pregnancy on neonatal body composition: A cross-sectional study.
Pacce, S, Saure, C, Mazza, CS, Garcia, S, Tomzig, RG, Lopez, AP, Ribarola, L, Krochick, GA
Diabetes & metabolic syndrome. 2016;(1 Suppl 1):S7-S12
Abstract
BACKGROUND The existence of early factors which, acting during critical periods of intrauterine or immediate postnatal development, determine long-term health has become increasingly recognized. Both high and low birth weight have been associated with cardiovascular risk factors in adulthood. Therefore, body composition at birth rather than birth weight may be a marker to predict future diseases. Maternal weight previous to and gained during pregnancy is associated with intrauterine fetal growth. OBJECTIVE To evaluate the correlation between maternal nutritional status before and during pregnancy and neonatal body composition. MATERIAL AND METHODS We studied consecutive mother-child pairs at delivery at an Argentinean public hospital during 5 months period, evaluating maternal and neonatal anthropometry before 24h of life as well as the history of the mother before and during pregnancy. Neonatal body composition was calculated according to a mathematical formula based on skinfold thickness measurement validated in newborns. RESULTS Mothers of newborns with high body fat mass were more frequently obese (72.7% versus 35.1%, p 0.005), and more frequently showed weight gain above 18kg during pregnancy (76.4% versus 31%, p 0.03). CONCLUSIONS Our findings confirm the hypothesis that maternal obesity before pregnancy is highly correlated with neonatal fat mass in the first hours of life.
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3.
Feeding Protocols for Neonates With Hypoplastic Left Heart Syndrome: A Review.
Jenkins, E
AACN advanced critical care. 2015;(3):215-21
Abstract
Optimizing nutrition in neonates with hypoplastic left heart syndrome is essential, given the high rate of growth failure in this population. Infants with hypoplastic left heart syndrome are predisposed to nutritional deficiency as a result of their increased metabolic demand; however, early enteral feeding also increases the risk of serious gastrointestinal morbidity and mortality caused by poor intestinal perfusion. Consequently, providers have difficulty deciding when and how to safely feed these patients. A review of the literature found that implementation of a structured enteral feeding protocol may decrease the risk of gastrointestinal complications while also minimizing dependence on parenteral nutrition and decreasing length of hospital stay. As these studies were limited, further research is warranted to establish a best practice feeding protocol to decrease risk and optimize nutrition in this fragile population.
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4.
Neonatal cardiovascular physiology.
Hines, MH
Seminars in pediatric surgery. 2013;(4):174-8
Abstract
The pediatric surgeon deals with a large number and variety of congenital defects in neonates that frequently involve early surgical intervention and care. Because the neonatal cardiac physiology is unique, starting with the transition from fetal circulation and including differences in calcium metabolism and myocardial microscopic structure and function, it serves the pediatric surgeon well to have a sound understanding of these principles and how they directly and indirectly affect their plans and treatments. In addition, many patients will have associated congenital heart disease that can also dramatically influence not only the surgical and anesthetic care but also the timing and planning of procedures. Finally, the pediatric surgeon is often called upon to treat conditions and complications associated with complex congenital heart disease such as feeding difficulties, bowel perforations, and malrotation in heterotaxy syndromes. In this article, we will review several unique aspects of neonatal cardiac physiology along with the basic physiology of the major groups of congenital heart disease to better prepare the training and practicing pediatric surgeon for care of these complex and often fragile patients.
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5.
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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6.
Hepatic function and physiology in the newborn.
Beath, SV
Seminars in neonatology : SN. 2003;(5):337-46
Abstract
The liver develops from progenitor cells into a well-differentiated organ in which bile secretion can be observed by 12 weeks' gestation. Full maturity takes up to two years after birth to be achieved, and involves the normal expression of signalling pathways such as that responsible for the JAG1 genes (aberrations occur in Alagille's syndrome), amino acid transport and insulin growth factors. At birth, hepatocytes are already specialized and have two surfaces: the sinusoidal side receives and absorbs a mixture of oxygenated blood and nutrients from the portal vein; the other surface delivers bile and other products of conjugation and metabolism (including drugs) to the canalicular network which joins up to the bile ductules. There is a rapid induction of functions such as transamination, glutamyl transferase, synthesis of coagulation factors, bile production and transport as soon as the umbilical supply is interrupted. Anatomical specialization can be observed across the hepatic acinus which has three distinct zones. Zone 1 borders the portal tracts (also known as periportal hepatocytes) and is noted for hepatocyte regeneration, bile duct proliferation and gluconeogenesis. Zone 3 borders the central vein and is associated with detoxification (e.g. paracetamol), aerobic metabolism, glycolysis and hydrolysis and zone 2 is an area of mixed function between the two zones. Preterm infants are at special risk of hepatic decompensation because their immaturity results in a delay in achieving normal detoxifying and synthetic function. Hypoxia and sepsis are also frequent and serious causes of liver dysfunction in neonates. Stem cell research has produced many answers to the questions about liver development and regeneration, and genetic studies including studies of susceptibility genes may yield further insights. The possibility that fatty liver (increasingly recognized as non-alcoholic steatohepatitis or NASH) may have roots in the neonatal period is a concept which may have important long-term implications.