Download or read book Maternal Obesity and Fetal Metabolic Programming Identifying a Role for Maternal Inflammation and Fetal Lipid Exposure written by Margaret J. R. Heerwagen and published by . This book was released on 2013 with total page 202 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal obesity is associated with greater risk of pregnancy complications. Additionally, children born to overweight and diabetic mothers are often large for gestational age, and at increased risk for developing metabolic syndrome later in life. It is thought that the intrauterine environment might be central to these observed outcomes, however, the particular characteristics of this environment remain elusive. The role of maternal lipids as a major contributor to fetal fat accretion is becoming increasingly recognized, but little is known about 1) the mechanisms regulating lipid transport across the placenta, and 2) how these lipids might impart persistent metabolic change on the fetus. Throughout the following work we address these questions in both human pregnancy and a high-fat diet mouse model of obese pregnancy. Our findings in humans suggest that placental growth and triglyceride hydrolase activity play an important role in regulating lipid flux to the developing fetus. In mice, our findings demonstrate how maternal obesity is complicated by increased maternal inflammation and insulin resistance, leading to placental overgrowth and increased lipid uptake. Further, these lipids appear to be transported to the fetus where they alter metabolic gene pathways and promote fetal hepatic lipid droplet accumulation. Lastly, we demonstrate that manipulating maternal dietary fatty acid profiles can alter this trajectory using a transgenic mouse model engineered to convert omega-6 fatty acids to omega-3 fatty acids. These mothers demonstrated reduced markers of systemic inflammation and improved insulin sensitivity, despite equivalent weight gain to wild type obese mothers. Additionally, placental growth was normalized and placental and fetal liver lipid exposure reduced. This resulted in either amelioration or complete prevention of adverse metabolic programming outcomes in wild type adult offspring. These results not only help us understand the interplay between pregnancy, diet, and obesity in regards to maternal lipid metabolism and fetal lipid exposure, but also suggest a potential means of protecting the developing fetus. A targeted intervention at the level of maternal and placental lipid metabolism is thus an important frontier in the quest for reducing fetal lipid exposure and the development of metabolic syndrome in children.

Download or read book Diet Nutrition and Fetal Programming written by Rajkumar Rajendram and published by Humana Press. This book was released on 2017-10-13 with total page 627 pages. Available in PDF, EPUB and Kindle. Book excerpt: This volume offers the most comprehensive coverage on fetal programming. Chapters are written by authors of international and national standing, leaders in the field and trendsetters. The clinical relevance of the current research is emphasized in each chapter, which also contains key points, key words, and concise summaries for ease of learning. Fetal programming affects conditions in the immediate postnatal period, as well as in later life and adulthood. These conditions include cardiovascular disease, frank hypertension, stroke, dyslipidemia, coagulopathy, increased insulin resistance-metabolic syndrome, type-2 diabetes, leukemia, testicular cancer, prostate cancer, breast cancer, polycystic ovary syndrome, precocious puberty, impaired immune function, renal disease, lung disease, and osteoporosis. Neuropathologies, behavioral and mental deficiencies, schizophrenia, and depression have also been reported in adults who were exposed to nutritional inadequacies in utero. Diet, Nutrition and Fetal Programming provides an overview on the effects of fetal programming on disease, and comprehensive looks at maternal nutrition factors and fetal programming effects on brain and behavior, and physiology and disease. It also provides an in depth look at specific nutrient restrictions and supplements on physiology and disease, the effects of maternal disease on fetal programming, mechanisms of programming, and a special section on the international aspects and policies on fetal programming.

Download or read book Obesity Before Birth written by Robert H Lustig and published by Springer Science & Business Media. This book was released on 2010-09-23 with total page 411 pages. Available in PDF, EPUB and Kindle. Book excerpt: This volume will explore the epidemiology and the basic mechanisms of each of these prenatal phenomena, in an attempt to explain the role of the prenatal environment in promoting postnatal weight gain. This information will contribute to resolving the nature-nurture controversy. This information provides guidance to clinical practitioners involved in both prenatal and postnatal care. This volume further stimulates research into underlying mechanisms and prevention and treatment of this phenomenon.

Download or read book Fetal and Early Postnatal Programming and its Influence on Adult Health written by Mulchand S. Patel and published by CRC Press. This book was released on 2017-07-12 with total page 776 pages. Available in PDF, EPUB and Kindle. Book excerpt: There is a documented link between fetal nutrition and the development of disease risk in adult life. Including the early postnatal period, during which a newborn continues to grow rapidly influenced by environmental factors, suggests that individuals are subject to risks for more than just the fetal period. Fetal and Early Postnatal Programming and its Influence on Adult Health focuses on interrelated aspects of cellular programming related to early nutrition and this potential global health problem.

Download or read book Maternal Obesity written by Matthew W. Gillman and published by Cambridge University Press. This book was released on 2012-07-19 with total page 265 pages. Available in PDF, EPUB and Kindle. Book excerpt: Afflicting more than 300 million women across the globe, obesity has profound effects on health during pregnancy and on the wellbeing of the unborn child. In the face of such a challenging pandemic, this book reviews the latest research and provides up-to-date advice on clinical management. Maternal Obesity addresses the adverse effects of obesity among women of childbearing age, including infertility, medical complications, problems in labor, and adverse birth outcomes, and it reviews evidence that the obese mother's in utero environment has long-lasting influences on the health of the developing child. Chapters cover basic, clinical, and population perspectives, providing a range of valuable information from mechanistic insight through to public health and policy implications. Invaluable for obstetricians, gynaecologists, paediatricians, general and family physicians, subspecialists in obstetric and paediatric medicine, midwives, and dietitians, as well as researchers and public health policy makers seeking to tackle the burden of maternal obesity-related illness.

Download or read book Maternal Obesity Programs Fetal Skeletal Muscle Development written by Xu Yan and published by . This book was released on 2011 with total page 261 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal obesity is associated with metabolic diseases such as obesity and type 2 diabetes (T2D) in offspring. Skeletal muscle is one of the principle sites for glucose and fatty acid oxidation, as well as the main tissue responding to insulin. Toll-like receptor 4 (TLR4) mediates chronic inflammatory signaling pathways and is associated with obesity and T2D. In the current study, we investigate the possible role of TLR4-mediated chronic inflammation in fetal skeletal muscle and intramuscular fat development, and the possible link of TLR4-mediated chronic inflammation to mitochondrial content and microRNA (miRNA) expression in fetal skeletal muscle. Using anobese sheep pregnancy model, we first analyzed whether the changes in obese (OB) fetal skeletal muscle we observed previously persist in the musculature of adult offspring. Consistent with our observations in fetal muscle, we observed elevated intramuscular adiposity and fibrosis in offspring muscle of over-nourished mothers, which was associated with attenuated insulin signaling and enhanced inflammatory signaling mediated by TLR4 when compared with control (Con) muscle. We propose that maternal obesity enhances adipogenesis and fibrogenesis in fetal and offspring muscle, which is expected to impair the physiological function of skeletal muscle. Next, we used a maternal nutrient excess (MNE) baboon pregnancy model and detected the mitochondrial content and function in fetal skeletal muscle at late gestation. Our results showed that the content of mitochondria was decreased in fetal skeletal muscle of MNE mothers compared with the control (CTR) group. Furthermore, genes related to mitochondrial biogenesis were expressed at a lower level in the MNE group. Similar to our sheep study, we also observed an elevated chronic inflammation in MNE fetal skeletal muscle, including the expression of TLR4. Therefore, we proposed a hypothetical model, in which we believe that MNE first induces the activation of chronic inflammation, which next affects the expression of genes involved in mitochondrial biogenesis, and then results in a decreased mitochondrial content in fetal skeletal muscle. Reduced mitochondrial content in fetal skeletal muscle might account for obesity and T2D in later life. In addition, we applied a miRNA microarray and analyzed the expression of miRNAs in fetal skeletal muscle during mid-gestation. We found more than 1,000 miRNAs expressing in sheep fetal skeletal muscle, of which several miRNAs were affected by maternal over-nutrition. Our results further showed that miRNA hsa-let-7g has a potential target which is involved in inflammation. So we over-expressed let-7g in C3H10T1/2 cells, which led to decreased expression of inflammatory cytokines TNF[alpha] and IL6, and inflammatory signaling mediator, TLR4. It is highly possible that miRNAs play some role in the development of chronic inflammation in fetal muscle of obese sheep. Meanwhile, we also found that miRNA let-7g inhibited the proliferation and adipogenic differentiation of C3H10T1/2 cells, suggesting an important role of miRNA let-7g in adipocyte development. Furthermore, we used a TLR4 knock out (KO) mouse model and assessed the role of TLR4 in pregnancy outcomes. Our data showed that TLR4 KO female mice were partially resistant to high fat diet (HFD)-induced obesity and insulin resistance. Meanwhile, TLR4 KO mice fed with HFD had a higher pregnancy rate and they were much better in taking care of their pups. In addition, the offspring of HFD TLR4 dams accumulated less subcutaneous and abdominal fat and had relatively higher insulin sensitivity compared with those of HFD C57 mice, especially female offspring. In summary, our results showed that maternal over-nutrition up-regulated the TLR4-mediated chronic inflammatory signaling in skeletal muscle of offspring. We further demonstrated that elevated inflammatory TLR4 signaling was associated with impaired mitochondria in fetal skeletal muscle in a primate model. Chronic inflammation and TLR4 signaling are partially regulated by miRNA let-7g in the sheep, since a lower level of let-7g was associated with elevated TLR4-mediated inflammatory signaling and over-expression of let-7g had anti-inflammatory effects. Chronic inflammation mediated by TLR4 may have a critical role in the development of fetal skeletal muscle and adipose tissue due to maternal obesity.

Download or read book Metabolic Syndrome and Complications of Pregnancy written by Enrico Ferrazzi and published by Springer. This book was released on 2015-06-24 with total page 237 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book explores the nature of pregnancy and metabolic syndrome as proinflammatory conditions and explains how pregnancy provides a window of opportunity for preventing the lifelong complications of metabolic syndrome, during which key risk factors can be identified and beneficial dietary changes can be implemented. The book’s opening sections discuss inflammation in the context of pregnancy, including the nature of the placenta as a proinflammatory tissue. In the main body, it points to new possible connections to truncal obesity, inflammation, metabolic syndrome, and major obstetrical syndromes, including preeclampsia, gestational diabetes and pre-term delivery. Based on the insights offered by this analysis, the remainder of the book focuses on a variety of nutritional measures and diets that can be of benefit during and beyond pregnancy. Readers will learn how the higher level of compliance with medical instructions during pregnancy can be capitalized on to ensure enduring health benefits for mother and child alike.

Download or read book The Role of Maternal High Fat Feeding on the Developmental Programming of Adulthood Disease written by Sarah Henry and published by . This book was released on 2014 with total page 340 pages. Available in PDF, EPUB and Kindle. Book excerpt: It is now well understood that the maternal environment encountered as a fetus can profoundly influence an individual's risk of developing a myriad of diseases in later life. In particular, maternal nutritional challenges can have significant developmental impacts to the fetus and this concept is generally referred to as the Developmental Programming of Adulthood Health and Disease. As many developed nations, including Australia, shift to states of nutritional excess, research focusing on adverse maternal conditions such as obesity, diabetes and high fat feeding is becoming critically relevant. Whilst numerous studies have begun to characterise the role of maternal obesity on offspring health, there is almost no understanding of how consumption of a maternal high fat diet, that does not cause frank obesity, might contribute to the programming of offspring health. Maternal obesity is not an isolated condition, and confounding factors such as altered hormonal profiles and gestational diabetes can make it difficult to delineate what factors are driving the varied developmental changes observed in offspring.While the longer term impacts of maternal high fat feeding on adult offspring is relatively well understood, there is limited information on the impact of high fat intake on the in utero environment, including the amniotic fluid and placenta. Furthermore, greater characterisation of the fetal phenotype is needed following maternal high fat feeding. In particular, limited information is available on the role of maternal fat intake and renal development. Finally, although several studies have assessed the role of maternal fat intake on aspects of postnatal vascular and cardiovascular function, adult renal function has not been fully assessed, despite strong evidence that disrupted renal development may increase the risk of developing disease in later life. AIMS & OBJECTIVES We aimed to investigate the impact of high maternal dietary saturated fat intake on fetal and postnatal development, including identifying the in utero adaptations to amniotic fluid lipid composition, fetal (including kidney) and placental growth and function. Long-term aims included investigation of the postnatal phenotype of offspring born to fat fed mothers, with particular focus on evaluating the long-term effects on renal, cardiovascular and sympathetic function.We hypothesised that maternal high fat feeding would modify placental transport of nutrients, resulting in a hyperlipidaemic fetal amniotic environment. As a result, fetal growth trajectory and organ development, specifically the kidneys, would be disrupted. Furthermore, we postulated that exposure to maternal high fat feeding would result in augmented blood pressure and renal dysfunction in offspring in later life and that increased sympathetic nerve activity may be responsible for these disruptions in physiological function. METHODS Investigations were carried out using Sprague-Dawley rats. For embryonic studies, female breeders were fed either a control (C; 7% canola oil) or a lard rich high fat (HF) (3% canola oil and 20% lard) diet for 3 weeks prior to mating and throughout pregnancy until embryonic day (E) 14.25, E17.25 or E20. At collection, embryos and placentas were weighed. Amniotic fluid and maternal plasma lipid profiles were determined using a lipidomics approach facilitated by liquid chromatography mass spectrometry (LCMS). Renal development was examined via culturing of embryonic kidneys and quantification of branching morphogenesis. In addition, gene expression of placental transporters and fetal liver substrates involved in lipid metabolism were determined using qPCR.For postnatal studies, female Sprague-Dawley rats were exposed to either C or HF diet for 3 weeks prior to mating, throughout pregnancy and lactation. From weaning, offspring were chow fed ad libitum. Physiological experiments were undertaken at 6 and 12 months of age. Renal glomerular filtration rate (GFR), effective renal plasma (eRPF) and blood flow (eRBF) were estimated in anaesthetized rats by 3H-inulin and 14C-para-aminohippurate clearance. Mean arterial pressure (MAP) and heart rate (HR) were determined in conscious animals using radiotelemetry. At 1 year of age, whole body noradrenaline spillover was estimated in anaesthetized rats. 3H-noradrenaline was infused and whole body noradrenaline spillover was calculated. Sodium nitroprusside (SNP) was then infused to determine changes in sympathetic arousal in response to acute hypotension. In addition, renal noradrenaline content was determined during development (E20) and in postnatal animals at 21 days and 1 year as a proxy measure of sympathetic nerve development and long-term sympathetic nerve activity respectively. RESULTS & DISCUSSION Maternal high fat feeding resulted in hyperlipidaemia, and this was reflected in amniotic fluid lipid content, with significant increases in amniotic fluid triglyceride concentrations in late gestation. In contrast to our hypothesis, fetal renal development did not differ between C and HF exposed embryos, however minor changes were observed in placental growth and transporter expression. These placental modifications do not fully explain the significant increases in amniotic fluid lipid content in late gestation. Further investigation indicated that increased fetal hepatic lipogenic gene expression was not a mechanism involved with increased triglyceride concentration in amniotic fluid.To further characterise our phenotype, development of offspring was followed into the postnatal period. We found that maternal high fat feeding was associated with significantly increased blood pressure in both male and female offspring at 12 months. In addition, sexually dimorphic renal dysfunction was evident in offspring of fat fed dams at 12 months of age. To our knowledge, this is one of the first studies to analyse renal function in a model of maternal high fat feeding, using gold standard techniques. Again, in contrast to our hypothesis, investigation into sympathetic nervous system revealed there was no difference in sympathetic activity between experimental groups, and that this was not a mechanism contributing to the renal and cardiovascular dysfunction in offspring exposed to in utero HF conditions. As such, it appears that other factors are driving the physiological dysfunction in this model. We hypothesise that vascular function may be impaired in HF exposed offspring and that this may be the major mechanisms driving the observed renal and cardiovascular dysfunction. CONCLUSION The findings from this thesis clearly demonstrate that even modest increases in saturated fat intake can alter the in utero environment, and the consequences of these early life modifications are seen in postnatal life, with significant renal and cardiovascular dysfunction. Importantly, this model of high fat feeding is not dissimilar to what many women are consuming during pregnancy - that is, the consumption of high saturated fats without apparent obesity. From an obstetrics perspective, it is clear that there is more to the picture than factors such as maternal obesity, and that dietary levels of saturated fatty acids should also be monitored. Whilst it appears that maternal obesity leads to a more severe phenotype in models of programming, high saturated fat intake during pregnancy cannot be ignored, and increased intake of this fatty acid has long term detrimental effects on the fetus.As we move to an increasing burden of chronic diseases, such as kidney and cardiovascular disease, it is vitally important to understand the impact of the early life environment on health and disease in later life. Furthermore, an understanding of the mechanism contributing to perturbed tissue and organ development may aid early intervention and as such disease prevention in later life. Controlling saturated fat intake during pregnancy may be a small but significant step in reducing the risk of developing adulthood diseases in later life.Finally, from a clinical perspective, the dietary model used in this project is not dissimilar to what many pregnant women in developed nations would be consuming. It highlights an important concept that women who consume a high fat diet during pregnancy, but do not develop obesity, are still placing the developing fetus at risk. Furthermore, it highlights that early intervention may be clinically important in potentially reducing the prevalence of adult chronic diseases.

Download or read book Fetal Cardiac Function written by E. Gratacós and published by S. Karger AG (Switzerland). This book was released on 2012 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Fetal echocardiography was initially used to detect structural anomalies, but has more recently also been proposed to assess fetal cardiac function. Functional echocardiography has been demonstrated to select high-risk populations and has been seen to have an effect on the outcome of several fetal conditions. Because of the small size and high heart rate and the restricted access away from the transducer, cardiovascular parameters should be validated but used with caution in the fetus. This special issue on fetal cardiac function is a collection of review and original articles showing several potential clinical and research applications of functional echocardiography in intrauterine growth restriction, twin-to-twin transfusion syndrome, congenital heart disease and aneuploides. The insights provided show that fetal cardiac function assessment is a promising tool that may soon be incorporated into clinical practice to diagnose, monitor or predict outcome in some fetal conditions. Therefore, this special issue on 'fetal cardiac function' provides valuable reading for clinicians and researchers in fetal medicine and cardiology who are interested in the fetal heart.

Download or read book The Role of Specific Maternal Nutritional Factors on Epigenetic Programming of Fetal Immune Development written by Nugegodage Dona Disanthi Manori Amarasekera and published by . This book was released on 2015 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: [Truncated] The burden of non-communicable diseases (NCD) including cardiovascular, metabolic, allergic and chronic lung diseases has reached pandemic proportions, as the major global health challenge in the 21st century. Understanding the causes and mechanisms of these diverse but pathogenically related inflammatory conditions remains a key challenge in overcoming these trends. The rise in these NCD is strongly related to modern lifestyle changes, and shared environmental risk factors, many of which disrupt early metabolic immune programming and predisposed to subsequent disease.The 'Developmental Origin of Health and Disease' (DOHaD) paradigm recognises the crucial importance of the early environment in shaping both structural, developmental and physiological response patterns in ways that may determine future health, biological reserve and disease susceptibility. Among many environmental exposures, the quality of early life nutrition is one of the most important factors influencing all aspects of development during critical formative periods, particularly during gestation. While the role of early metabolic adaptations has been long recognised as a predisposing factor, the impact of the early environment on the developing immune system in the subsequent predisposition to inflammation, has only been recognised more recently. Identifying and optimising early factors that influence the patterns of immune development is central in understanding disease pathogenesis and in implementing better prevention strategies. In particular, variations in maternal nutrition can significantly modify both immune and metabolic programming, to determine the long-term health outcomes of the offspring. Only recently has it been recognised that many of these effects are mediated through epigenetic mechanisms such as DNA methylation and histone acetylation. The strong link between changes in the modern diet and escalating rate of allergic and other NCD underscores the importance of identifying specific in utero nutritional exposures affecting the fetal epigenome leading to an altered immune profile.

Download or read book Weight Gain During Pregnancy written by National Research Council and published by National Academies Press. This book was released on 2010-01-14 with total page 868 pages. Available in PDF, EPUB and Kindle. Book excerpt: As women of childbearing age have become heavier, the trade-off between maternal and child health created by variation in gestational weight gain has become more difficult to reconcile. Weight Gain During Pregnancy responds to the need for a reexamination of the 1990 Institute of Medicine guidelines for weight gain during pregnancy. It builds on the conceptual framework that underscored the 1990 weight gain guidelines and addresses the need to update them through a comprehensive review of the literature and independent analyses of existing databases. The book explores relationships between weight gain during pregnancy and a variety of factors (e.g., the mother's weight and height before pregnancy) and places this in the context of the health of the infant and the mother, presenting specific, updated target ranges for weight gain during pregnancy and guidelines for proper measurement. New features of this book include a specific range of recommended gain for obese women. Weight Gain During Pregnancy is intended to assist practitioners who care for women of childbearing age, policy makers, educators, researchers, and the pregnant women themselves to understand the role of gestational weight gain and to provide them with the tools needed to promote optimal pregnancy outcomes.

Download or read book Physical Activity and Maternal and Neonatal Outcomes in Obese Pregnant Women written by Rachel Ann Tinius and published by . This book was released on 2015 with total page 164 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal obesity and physical inactivity during pregnancy are independently associated with unfavorable maternal and neonatal metabolic outcomes. Previous research in non-gravid adults suggests physical activity provides protection from many chronic diseases irrespective of body weight. The primary purposes of this dissertation were to determine the impact of obesity on maternal metabolic health (lipid metabolism, inflammation, insulin resistance) and neonatal metabolic health (adiposity, inflammation, insulin resistance), and to determine if adverse maternal and neonatal metabolic health is improved in obese pregnant women who are physically active during pregnancy compared to sedentary obese women. The secondary purpose of this dissertation was to examine the relationships between maternal and neonatal metabolic health. Three groups of pregnant women were compared between 32 and 37 weeks gestation (N=50). Groups consisted of: 1) lean women, 2) obese sedentary women, and 3) obese physically active women. Body composition (skinfold anthropometry), physical fitness levels (submaximal cycle test), and physical activity levels (accelerometry) were assessed. Maternal plasma markers of insulin resistance (Homeostatic Model Assessment-Insulin Resistance (HOMA-IR)) and systemic inflammation (C -- reactive protein) were measured at rest. Lipid oxidation rate and lipolysis were measured at baseline, during a 30-minute bout of low-intensity exercise, and during a 1-hour recovery period. Cord blood was collected at parturition to measure neonatal plasma insulin resistance, inflammation, and free fatty acid concentration. Neonatal body composition was measured 24-48 hours postpartum via skinfold anthropometry and air displacement plethysmography. In Chapter 2, maternal and neonatal outcomes were compared between lean and obese pregnant women. Obese pregnant women had higher maternal inflammation, insulin resistance, and lipid oxidation rates. Maternal lipid oxidation rate and inflammation were positively correlated. Maternal inflammation was positively correlated to insulin resistance and blood pressure. Therefore, lipid metabolism may be contributing to inflammation and subsequent insulin resistance and hypertension in obese pregnant women. In Chapter 3, maternal and neonatal outcomes were compared between obese sedentary and obese physically active pregnant women. Physically active obese women had lower systemic inflammation compared to sedentary obese women; thus, regular physical activity may improve inflammation in obese pregnant women. In Chapter 4, the relationships between maternal and neonatal metabolic outcomes were examined. There were no correlations between maternal and neonatal metabolic outcomes across all women in the study. Several relationships between maternal and neonatal outcomes were found when comparing lean or obese women separately, which suggests that the mechanisms linking maternal and neonatal metabolic health are complex and potentially BMI-dependent. In Chapter 5, the relationship between intensity of physical activity and maternal inflammation was examined. Low-intensity physical activities had the strongest negative correlation to systemic inflammation. Data from Chapter 5 also suggest that small daily increases in low-intensity physical activities may be enough of a stimulus to elicit clinically meaningful reductions in inflammation. Thus, pregnant women should be encouraged to participate in low-intensity physical activities in order to reduce their systemic inflammation and improve their long-term health. Overall, results from this dissertation project suggest that obesity during pregnancy has unfavorable implications for maternal metabolic health. However, a physically active lifestyle might mitigate these alterations, particularly maternal systemic inflammation. Pregnant women of all body weights should be encouraged to participate in daily physical activity, even low-intensity activity, in order to improve their health and the future health of their offspring.

Download or read book Fetal Programming of Obesity and Metabolic Dysregulation by Maternal Nutrition written by Lindsey Ann George and published by . This book was released on 2010 with total page 198 pages. Available in PDF, EPUB and Kindle. Book excerpt: Increased risk for obesity and metabolic disease has been attributed to both maternal overnutrition and undernutrition in pregnancy. Obesity and metabolic disease are components of the metabolic syndrome which predisposes to development of more severe disease, including cardiovascular disease and type II diabetes. This dissertation discusses studies using a sheep model to evaluate the effects of maternal overnutrition on fetal development and maternal undernutrition on offspring disease risk. In the first experiment, ewes were fed to achieve normal weight, overweight or obesity prior to and during pregnancy. The most overfed ewes became fattest by the time of breeding which was associated with increased fetal adiposity and organ growth at mid-gestation. In the second experiment, aged ewe offspring born from mothers nutrient restricted in early gestation were evaluated for differences in feeding behavior, glucose-insulin dynamics and body composition during a bout of ad libitum feeding. These aged (6 yrs) ewe offspring of nutrient restricted mothers demonstrated greater and more rapid feed intake, greater body weight gain and gain efficiency, as well as lower insulin sensitivity and higher insulin secretion than control ewe offspring. In the third experiment, these same aged ewe offspring from nutrient restricted dams showed lower progesterone concentrations throughout the estrous cycle, a result previously observed in these ewes at one and two years of age, indicating progesterone levels have been permanently programmed in these ewes. Overall, fetal programming of disease risk related to metabolic disease and obesity has been demonstrated in our ewe model of both maternal under- and overnourishment.

Download or read book Handbook of Life Course Health Development written by Neal Halfon and published by Springer. This book was released on 2017-11-20 with total page 667 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is open access under a CC BY 4.0 license. ​This handbook synthesizes and analyzes the growing knowledge base on life course health development (LCHD) from the prenatal period through emerging adulthood, with implications for clinical practice and public health. It presents LCHD as an innovative field with a sound theoretical framework for understanding wellness and disease from a lifespan perspective, replacing previous medical, biopsychosocial, and early genomic models of health. Interdisciplinary chapters discuss major health concerns (diabetes, obesity), important less-studied conditions (hearing, kidney health), and large-scale issues (nutrition, adversity) from a lifespan viewpoint. In addition, chapters address methodological approaches and challenges by analyzing existing measures, studies, and surveys. The book concludes with the editors’ research agenda that proposes priorities for future LCHD research and its application to health care practice and health policy. Topics featured in the Handbook include: The prenatal period and its effect on child obesity and metabolic outcomes. Pregnancy complications and their effect on women’s cardiovascular health. A multi-level approach for obesity prevention in children. Application of the LCHD framework to autism spectrum disorder. Socioeconomic disadvantage and its influence on health development across the lifespan. The importance of nutrition to optimal health development across the lifespan. The Handbook of Life Course Health Development is a must-have resource for researchers, clinicians/professionals, and graduate students in developmental psychology/science; maternal and child health; social work; health economics; educational policy and politics; and medical law as well as many interrelated subdisciplines in psychology, medicine, public health, mental health, education, social welfare, economics, sociology, and law.

Download or read book Human Maternal Obesity in the Development of Nonalcoholic Fatty Liver Disease in a Germ free Mouse Model written by Taylor Kristina Soderborg and published by . This book was released on 2019 with total page 223 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal metabolism and obesity contribute significantly to the risk of obesity and non-alcoholic fatty liver disease (NAFLD) in the next generation, however the causal drivers of this relationship are currently unclear. Metabolic diseases in the pediatric population pose a unique challenge as the mechanisms driving their onset and progression are hypothesized to be the result of programming by early life exposures in addition to lifestyle factors. The earlier onset of obesity and NAFLD in the pediatric population is associated with a worse natural history and progression of these conditions compared to adults. At the time of diagnosis, half of pediatric patients have the more progressive, inflammatory version of NAFLD, non-alcoholic steatohepatitis (NASH), and those diagnosed in childhood have a worse prognosis that adults. Despite the alarming rate of pediatric NAFLD worldwide, particularly in obese youth, at present there are no interventions that have convincingly demonstrated efficacy to alter the progression of this disease. Importantly, given the involvement of inflammation in pediatric NASH, as demonstrated by a unique periportal inflammation, it is likely that the pathogenesis of NAFLD in children may have distinct features from that in adults. Evidence of leaky gut barriers in children with NASH in addition to histological evidence portal inflammation, suggests that the early gut microbiome may play a significant role in pediatric NAFLD. Early life dysbiosis has been found in offspring of obese and/or high fat diet fed mothers in both human, non-human primate and murine models. Research in humans also suggests that excessive gestational weight gain (EWG) and gestational diabetes mellitus (GDM) can also influence offspring microbiome composition. However, there are very limited prospective human data on the influence of commonly co-morbid metabolic conditions, such as EWG and obesity, or, GDM and obesity, on offspring gut colonization. Importantly, while there is correlative data associating early dysbiosis with worse metabolic outcomes in human offspring, causality has not yet been established. Throughout the following work we build upon the existing knowledge of how maternal phenotype influences human offspring microbiome composition and develop mechanistic connections between the altered gut microbiota and metabolic disease risk in a germ-free mice model. We demonstrate in a germ-free mouse model a causative role for this dysbiosis in predisposition to obesity and NAFLD upon exposure to a western style diet. Specifically, we discovered that dysbiosis results in a hypo-responsive bone marrow derived macrophage with dysfunction of both classical and alternative metabolism in a germ-free mouse model. Similar to the influence of maternal obesity on the human infant gut microbiome, we find that EWG and GDM independently and through their interaction with obesity, uniquely influence the composition of the human offspring microbiome at 2 weeks of life. Our findings suggest that maternal metabolic phenotype influences the colonization of the early human infant gut with lasting alterations of the innate immune system, as suggested by our germ-free mouse model. These results expand upon the current understanding of how maternal metabolic obesity, EWG and GDM in humans influences the human offspring gut microbiome and also provide insight to the mechanism by which maternal obesity could potentially cause NAFLD, as demonstrated in germ-free mice. This work supports targeting the early life microbiome in the development of effective preventative measures to impair the perpetuation of metabolic disease in the next generation.

Download or read book Military Strategies for Sustainment of Nutrition and Immune Function in the Field written by Institute of Medicine and published by National Academies Press. This book was released on 1999-05-13 with total page 722 pages. Available in PDF, EPUB and Kindle. Book excerpt: Every aspect of immune function and host defense is dependent upon a proper supply and balance of nutrients. Severe malnutrition can cause significant alteration in immune response, but even subclinical deficits may be associated with an impaired immune response, and an increased risk of infection. Infectious diseases have accounted for more off-duty days during major wars than combat wounds or nonbattle injuries. Combined stressors may reduce the normal ability of soldiers to resist pathogens, increase their susceptibility to biological warfare agents, and reduce the effectiveness of vaccines intended to protect them. There is also a concern with the inappropriate use of dietary supplements. This book, one of a series, examines the impact of various types of stressors and the role of specific dietary nutrients in maintaining immune function of military personnel in the field. It reviews the impact of compromised nutrition status on immune function; the interaction of health, exercise, and stress (both physical and psychological) in immune function; and the role of nutritional supplements and newer biotechnology methods reported to enhance immune function. The first part of the book contains the committee's workshop summary and evaluation of ongoing research by Army scientists on immune status in special forces troops, responses to the Army's questions, conclusions, and recommendations. The rest of the book contains papers contributed by workshop speakers, grouped under such broad topics as an introduction to what is known about immune function, the assessment of immune function, the effect of nutrition, and the relation between the many and varied stresses encountered by military personnel and their effect on health.

Download or read book Maternal Fetal Nutrition During Pregnancy and Lactation written by Michael E. Symonds and published by Cambridge University Press. This book was released on 2010-01-28 with total page 217 pages. Available in PDF, EPUB and Kindle. Book excerpt: With the aim to improve clinicians' understanding of the important effects nutrition can have on maternal health and fetal and neonatal development, Maternal-Fetal Nutrition During Pregnancy and Lactation defines the nutritional requirements with regard to the stage of development and growth, placing scientific developments into clinical context.