Download or read book What are the Effects of Maternal Obesity on Synaptic Function in the Maternal and Offspring Hippocampus written by Denise Lau and published by . This book was released on 2013 with total page 99 pages. Available in PDF, EPUB and Kindle. Book excerpt: Obesity is a global epidemic that is associated with several adverse health consequences. In addition, there is also a growing prevalence of obesity in pregnancy. Maternal obesity places the fetus in an abnormal in utero condition that can produce alterations in development leading to permanent programming of physiological systems. Obesity is also associated with cognitive dysfunction, which calls for investigations into its effects on the hippocampus, a brain area involved in learning and memory. Long-term potentiation (LTP), a neurophysiological correlate for learning and memory, can be examined in hippocampal slices. This study aimed to fill in the gap in literature regarding the effect of obesity on hippocampal synaptic plasticity in female rats, and maternal obesity effects on offspring hippocampal synaptic plasticity. Female Sprague-Dawley rats were fed either a control diet (CD), or a high-fat diet (HFD; 40% of calories from saturated fat) for 16 weeks. Impaired glucose tolerance and greater retroperitoneal fat pad weight indicated an obese phenotype in HFD rats; as well, the modified diet led to impaired LTP: CD rats had 10% more potentiation in amplitude, and 11% more potentiation in slope than HFD rats. Offspring were weaned onto control diet at post-natal day 21. Reduced success rates for achieving LTP, and lowered magnitudes of mean LTP in the offspring, strongly suggest that maternal obesity may have compromised hippocampal synaptic plasticity, and warrants further study.

Download or read book Effects of Maternal High Fat Diet Consumption on Offspring Letpin Signaling and Brain Development written by Sophie Corinne Trombetta and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

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 Does Maternal Obesity Affect Hippocampal dependent Spatial Learning and Memory Retention in Offspring written by Jamie-Lee Robb and published by . This book was released on 2015 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Prenatal Maternal Infection and Synaptic Transmission in the Hippocampus written by Germaine Lowe and published by . This book was released on 2011 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: The hippocampus, which plays a crucial role in cognitive processes, is a brain region that has been repeatedly shown to be disrupted in schizophrenia, which likely contributes to some of the cognitive impairments associated with the disease. Although the aetiology of schizophrenia remains unknown, mounting evidence from epidemiological studies have implicated exposure to infection during pregnancy as a potent risk factor for schizophrenia in the offspring. Using rodent models to mimic maternal infection during gestation, we sought to examine in the offspring changes that may be occurring in the hippocampus. While anatomical and behavioural alterations have been reported in the hippocampus in rodent models of prenatal maternal infection, it remains unknown as to how hippocampal synaptic transmission is affected. Understanding what is occurring at the synaptic level will help to understand the consequences of maternal infection during pregnancy on hippocampal...

Download or read book The Impact of Maternal Nutrition on the Offspring written by Gerard Hornstra and published by Karger Medical and Scientific Publishers. This book was released on 2005-01-01 with total page 273 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal nutritional status affects the offsprings health development significantly during early embryogenesis, pregnancy, birth and lactation, and subsequently determines health during growth and even throughout adulthood. On the other end of the human lifetime scale, the importance of maternal nutrition expands into the time period before conception: Pre-conception nutritional status not only influences fertility, but also embryogenesis and life-long health. Predisposition for coronary heart diseases, Type-2 diabetes mellitus, and hypertension can be caused by intrauterine adaptations to fetal malnutrition. Hence, optimizing nutrition for women during their reproductive period can be expected to have a great impact on the well being of the next generation. This workshop dealt with the effects of maternal nutrition on fetal growth, metabolic programming, energy and nutrient requirements, as well as under- and over-nutrition during pregnancy. Finally, it addressed the question of whether a distinct diet during pregnancy could reduce food allergy in the progeny. This book is a valuable and complete source of knowledge for all professionals involved in pediatrics, nutrition policy, womens health, immunology, epidemiology and public health.

Download or read book The Effects of High fat Feeding on Synaptic Function in Female Rats and Their Offspring written by Isabelle Lorraine Messa-Hamidi and published by . This book was released on 2014 with total page 87 pages. Available in PDF, EPUB and Kindle. Book excerpt: The prevalence of obesity has been increasing across the globe at an unprecedented rate, and obesity is associated with a number of diseases, including diabetes, hypertension, and certain types of cancer. In recent years, increasing evidence has shown that obesity can also cause cognitive impairment, and research is increasingly aimed at elucidating both the nature of, and the mechanisms behind, these impairments in the brain. Because the hippocampus has been shown to be particularly vulnerable to these effects, both of the studies presented in this thesis aimed to investigate the effects of high-fat diet-induced obesity on hippocampal synaptic plasticity.

Download or read book Acute and Maternal Effects of a High Fat Diet written by Emily Rose Trunnell and published by . This book was released on 2016 with total page 334 pages. Available in PDF, EPUB and Kindle. Book excerpt: Obesity is one of the leading drivers of healthcare costs associated with preventable chronic disease. On average, U.S. adults gain on average 0.4 to 1 kg per year and it is likely that much of this annual weight gain is an additive result of short-term dietary excess. A significant factor driving short-term weight gain is overconsumption of foods high in fat. Even prior to weight gain, high dietary fat consumption can induce metabolic and physiological changes that are predictive of future weight gain and disease. Animal models used to study the effects of dietary manipulations have paid particular attention to the impact of diet on the brain; however the impact of acute fat intake on the brain has been less well studied. The following chapters provide a rationale for studying the impact of high fat diet on the hippocampus, a brain structure important for learning and memory, and supply novel evidence that acute high fat diet consumption alters hippocampal gene transcription as well as behavior in rats. Finally, we show that exposure to a high fat diet prior to weaning impacts the hippocampal gene expression in mouse offspring in a sex- and time-specific manner.

Download or read book Maternal Obesity Alters Fetal Development Due to Impaired Placental Function and Has Lasting Effects on Adult Offspring written by Kristin Norwood and published by . This book was released on 2013 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book The Effect of Maternal Obesity on Offspring Neurodevelopmental Outcomes written by Julie Sigurdardottir and published by . This book was released on 2022 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Cardiovascular and Multigenerational Implications of Maternal Obesity written by Christopher L. Pankey and published by . This book was released on 2018 with total page 106 pages. Available in PDF, EPUB and Kindle. Book excerpt: Obesity is a growing global issue associated with adverse health consequences including cardiovascular disease, the leading cause of death worldwide. According to the World Health Organization, global obesity has tripled since 1975, and 41 million children under five were obese or overweight in 2016. Sedentary lifestyle and hypercaloric diets are key contributors to increasing incidence of obesity, but there are additional contributing factors to consider. Previous studies from our lab have shown that maternal obesity (OB) predisposes offspring to exhibit indications of the metabolic syndrome including insulin/glucose dysregulation, increased adiposity, hypercortisolemia, and cardiovascular disease. These findings are supported by multiple epidemiologic and controlled animal studies. However, many questions remain regarding in vivo cardiovascular function, and intergenerational programming effects. This dissertation focuses on the intergenerational and transgenerational programming of adverse cardiovascular and metabolic phenotypes from OB. In the first experiment, we evaluated in vivo cardiovascular structure and function using invasive blood pressure measurements, and echocardiography. We found that in prenatal life, OBF1 fetuses have thicker aortas, with a greater collagen:elastin ratio (suggestive of lowered elasticity). We also found that OBF1 are hypertensive relative to CONF1 at 2.5 months of age, yet hypotensive with multiple cardiac geometric changes upon reaching advanced age. These findings suggest that OB programs vascular changes that increase cardiac workload in the young, and eventually leads to indications of cardiac failure in old age. The second and third studies focus on inter- and transgenerational programming of indications for metabolic syndrome after OB. We found that intergenerational programming resulted in OBF2 exhibiting insulin/glucose dysregulation, hypercortisolemia, and increased weight gain when F2 were exposed to a metabolic stress such as ad libitum feed or gestation. We also found that OBF3 show differences in body size and weight at birth, but seemingly normal endocrine profiles. These data suggest that OB programs transgenerational phenotypes that may be epigenetically linked, yet many phenotypes require direct exposure to the initial OBF0 uterine environment. Given the similarities of fetal:maternal mass, temporal pattern of development, and precocial offspring, we suggest that this model is imperative to improving our understanding of obese pregnancies in humans.

Download or read book Vibrant and Healthy Kids written by National Academies of Sciences, Engineering, and Medicine and published by National Academies Press. This book was released on 2019-12-27 with total page 621 pages. Available in PDF, EPUB and Kindle. Book excerpt: Children are the foundation of the United States, and supporting them is a key component of building a successful future. However, millions of children face health inequities that compromise their development, well-being, and long-term outcomes, despite substantial scientific evidence about how those adversities contribute to poor health. Advancements in neurobiological and socio-behavioral science show that critical biological systems develop in the prenatal through early childhood periods, and neurobiological development is extremely responsive to environmental influences during these stages. Consequently, social, economic, cultural, and environmental factors significantly affect a child's health ecosystem and ability to thrive throughout adulthood. Vibrant and Healthy Kids: Aligning Science, Practice, and Policy to Advance Health Equity builds upon and updates research from Communities in Action: Pathways to Health Equity (2017) and From Neurons to Neighborhoods: The Science of Early Childhood Development (2000). This report provides a brief overview of stressors that affect childhood development and health, a framework for applying current brain and development science to the real world, a roadmap for implementing tailored interventions, and recommendations about improving systems to better align with our understanding of the significant impact of health equity.

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 The Impact of Diabetes on Hippocampus written by Saeed Vafaei-Nezhad and published by . This book was released on 2019 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal Diabetes is one of the most common metabolic disorders resulting an increased risk of abnormalities in the developing fetus and offspring. It is estimated that the prevalence of diabetes during pregnancy among women in developing countries is approximately 4.5 percent and this range varies between 1 to 14 percent in different societies. According to earlier studies, diabetes during pregnancy is associated with an increased risk of maternal and child mortality and morbidity as well as major congenital anomalies including central nervous system (CNS) in their offspring. Multiple lines of evidence have suggested that infants of diabetic women are at risk of having neurodevelopmental sequelae. Previous studies reveal that the offspring of diabetic mothers exhibit disturbances in behavioral and intellectual functioning. In the examination of cognitive functioning, a poorer performance was observed in the children born to diabetic mothers when compared with the children of non-diabetic mothers. Therefore, it is important to study the possible effects of maternal diabetes on the hippocampus of these infants.

Download or read book The impact of maternal obesity on vascular and metabolic function throughout pregnancy written by Frances Maria Stewart and published by . This book was released on 2008 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Maternal Obesity AMP activated Protein Kinase and Fetal Skeletal Muscle Development written by Junfeng Tong and published by . This book was released on 2010 with total page 263 pages. Available in PDF, EPUB and Kindle. Book excerpt: Maternal obesity during gestation programs offspring to obesity and type 2 diabetes in adulthood. Skeletal muscle is the major peripheral tissue responsive to insulin. The prenatal stage is crucial for skeletal muscle development. AMP-activated protein kinase (AMPK) is involved in both skeletal muscle development and etiology of obesity. In this study, we investigated the effects of maternal obesity on fetal skeletal muscle development, AMPK activity, and their association with fetal origins of obesity and type 2 diabetes. Using the obese pregnant ewe model, we showed that myogenesis was attenuated and the diameter of primary muscle fibers was smaller in fetal skeletal muscle born to obese dams (OB). Wingless and Int (Wnt)/[beta]-Catenin signaling pathway promotes myogenesis and inhibits adipogenesis. The Wnt/[beta]-catenin signaling was down-regulated in OB fetal muscle, which was associated with inflammatory response in fetal muscle due to maternal obesity. Moreover, AMPK activity was reduced while the expression of adipogenic marker peroxisome proliferator-activated receptor (PPAR) [gamma] was increased in OB fetal muscle. In 3T3-L1 cell lines, pharmacological activation of AMPK inhibited the expression of PPAR[gamma] and reduced the presence of adipocytes, while pharmacological inhibition of AMPK enhanced the expression of PPAR[gamma]. These data suggest that AMPK activity is inversely related to adipogenesis in fetal sheep muscle and 3T3-L1 cells. In the diet-induced obesity mouse model, we also observed the down-regulation of AMPK activity, myogenic markers, and mitochondrial content and function, while the up-regulation of PPAR[gamma] in the skeletal muscle of offspring born to obese dams (OB). Maternal metformin administration to obese mice during gestation and lactation activated AMPK activity and prevented these changes in OB offspring skeletal muscle, which suggested that maternal administration of metformin might improve OB offspring muscle function. Besides, we investigated the role of AMPK in skeletal muscle protein degradation in C2C12 myotubes. The data showed that pharmacological activation of AMPK stimulated two muscle specific ubiquitin ligases expression, indicating that acute AMPK activation may promote muscle protein degradation. In summary, our data show that maternal obesity affects fetal skeletal muscle development which has long-term effects on offspring properties, and AMPK is a key mediator affecting fetal skeletal muscle development.

Download or read book Developmental Programming Effects of Maternal Obesity written by Carolle Kassab and published by . This book was released on 2020 with total page 12 pages. Available in PDF, EPUB and Kindle. Book excerpt: Population studies within the United States indicate increasing rates of obesity, considerably prominent for women within reproductive age. Maternal obesity is associated with the offspring's hyperlipidemia, diabetes, and cardiovascular disease, which have chronic consequences. Obesity in pregnancy causes metabolic and epigenetic perturbations within the fetal environment, disrupting future health of offspring. This phenomenon is known as developmental programming. Although the relationship between maternal undernutrition and developmental programming has been demonstrated, its relationship to maternal obesity remains understudied.