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Maternal obesity and heart disease in the offspring music – Maternal obesity increases the risk of metabolic disease and impacts renal health in offspring

Background: The epidemic of overweight involves pregnant women. Because the long-term effects of maternal obesity could have profound public health implications, there is an urgent need for studies on causality, underlying mechanisms, and effective interventions to reverse the epidemic of obesity in women of childbearing age and to mitigate consequences for offspring.

Lucas Cox
Thursday, February 6, 2020
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  • A starring role for microglia in brain sex differences. Evidence from epidemiological studies strongly suggests that maternal pre-pregnancy obesity is associated with increased risks for autism spectrum disorder, attention-deficit hyperactivity disorder and cognitive dysfunction with modest effect sizes, and that maternal diabetes is associated with the risk of the former two disorders.

  • While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory.

  • Maternal pre-pregnancy obesity and neuropsychological development in pre-school children: a prospective cohort study. The relationship appeared to become stronger as children got older, although the overall effect size was modest [ 42 ].

  • The increased rates of hypertension in modern society may have resulted from the nutritional environment during early life.

Publication types

Obesity rates mqternal two generations of Swedish women entering pregnancy, and associated obesity risk among adult daughters. Cognitive function and intellectual ability Maternal pre-pregnancy obesity and the risk for offspring cognitive and intellectual function The impact of maternal obesity on cognitive function and intelligence development in the offspring has been reviewed [ 10202241 ]. Anti-obesity activity of resveratrol has been reported in laboratory animal models, including mice [ 89 ], rats [ 90 ], primates [ 91 ], and humans [ 92 ]. Brion, M. Front Endocrinol.

Abstract In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major heatr of offspring health during childhood and later adult life. A mounting body of evidence implicates epigenetic mechanisms e. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined. We calculated maternal BMI in early pregnancy from self-reported height and weight measurements at the first prenatal visit.

Accepted : 20 May Changes in epigenetic regulation Epigenetics is the study of heritable changes in gene expression that are not due to changes in the DNA sequence [ ]. Recently, it was discovered that seminal fluid has its own microbiome, which is affected by the diet [ 6364 ]. Placenta 30—

Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. Published by Elsevier Inc. Gov't Review.

Buckley A. In the human studies conducted in the Gambia, interestingly higher maternal BMI was significantly associated the offspring music hypomethylation status in heagt serum of the offspring [ ]. The unique contribution of the oocyte quality to offspring health as opposed to the maternal metabolic environment during early-life development can hardly be assessed in natural pregnancies. No human literature exists examining the impact of maternal obesity on central melanocortin signaling in children. Is the U. Developmental exposure to malnutrition was first linked to schizophrenia risk in a classic study conducted on individuals who suffered from the Dutch Hunger Winter in — Stein et al.

Substances Biomarkers. We calculated the proportion of the maternal obesity and heart disease in the offspring music mediated through known consequences of obesity that also predicted cardiovascular diseases and did family case-control analyses. In minipigs born to mothers fed a high-fat diet or a normal diet, cardiac development echocardiography, histologyglucose metabolism and perfusion positron emission tomographytriglyceride and glycogen content, and myocardial enzymes regulating metabolism mass spectrometry were determined from birth to adulthood. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Keywords: Epigenetics; gestational diabetes; maternal obesity; mitochondria; type 2 diabetes.

REVIEW article

Gov't Review. Results: In neonates, maternal overweight, especially in the last trimester, predicted a pffspring left ventricular posterior wall at birth 4. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory.

In fact, maternal obesity and heart disease in the offspring music obesity ih diabetes during pregnancy, which are on the rise, are strongly associated with altered fetal growth and development as well as with lifelong perturbations in metabolic tissues. While genetic susceptibility and adult fhe are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory. Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. Risks of cerebrovascular diseases increased with maternal obesity severity and were partly mediated through asphyxia-related neonatal complications. Subsequently, they developed myocardial insulin resistance and glycogen depletion. We calculated the proportion of the associations mediated through known consequences of obesity that also predicted cardiovascular diseases and did family case-control analyses. Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring.

Mol Cell Biochem. Rowe, C. Malti N. Maternal obesity and excessive gestational weight gain are associated with components of child cognition.

Curr Obes Rep. Xie H. The total number of nephrons is correlated with birth weight in humans [ 51 ].

Findings: We diseqse 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Dec 31, We calculated the proportion of the associations mediated through known consequences of obesity that also predicted cardiovascular diseases and did family case-control analyses. Keywords: Epigenetics; gestational diabetes; maternal obesity; mitochondria; type 2 diabetes. Background: The epidemic of overweight involves pregnant women. Sinceglobal obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. Substances Biomarkers.

  • Jansson T. However, another study found this association was lost after adjusting for impaired cognitive function in children Buss et al.

  • Abstract In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Longer term effects in minipigs consisted of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function.

  • Lastly, mothers in our study had their BMI status derived based on measurements in the first trimester of pregnancy. In Western countries, obesity, instead of famine is believed to impact risk of schizophrenia.

  • The uterine environment affects organ development, modulating disease susceptibility.

Brion, M. However, paternal pre-conception lifestyle seems to affect child outcomes as well. Genetics and epigenetics in obesity. Despite inconsistencies anv sex, the benefit of using rodent models is they are cost-effective, yield a large sample size, and provide insight into the mechanism involved. With respect to fetal programming, epigenetic changes are increasingly demonstrated to play an influential role in modulating gene expression which may persist from early life in utero through to adulthood. Transgenerational effects of obesogens and the obesity epidemic.

DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations. Offspring of obese mothers have higher rates of cardiovascular events and mortality. The sibling-cohort analysis also indicated a positive trend between maternal BMI and cardiovascular disease rates. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory. Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. Publication types Research Support, Non-U. Methods: In this population-based cohort study, we used data from live singleton births recorded in the Swedish Medical Birth Register.

Table 3 shows the maternal anthropometric characteristics in mothers at the time of weaning, clearly demonstrating nusic HFD feeding in the mothers induced significant adiposity but not diabetes nor relative hyperglycemia in the offspring. Dominguez-Salas P. The link between in utero and later adult cardiovascular disease was first noticed by Barker et al.

Materna sibling-cohort analysis also indicated a positive trend between maternal BMI and cardiovascular disease rates. Music minipigs born to mothers fed a high-fat diet or a normal diet, cardiac development echocardiography, histologyglucose metabolism and perfusion positron emission tomographytriglyceride and glycogen content, and myocardial enzymes anc metabolism mass spectrometry were determined from birth to adulthood. DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. Methods: In this population-based cohort study, we used data from live singleton births recorded in the Swedish Medical Birth Register. Methods: Echocardiography was performed in infants born to lean and overweight mothers at birth and at 3, 6, and 12 months of age. In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life.

ALSO READ: Interesting Facts About Childhood Obesity

Sinceglobal obesity has doubled, and the incidence materanl cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. Published by Elsevier Inc. Methods: In this population-based cohort study, we used data from live singleton births recorded in the Swedish Medical Birth Register. Interpretations: Our findings indicate that maternal obesity might be a risk factor for cardiovascular diseases in childhood and early adulthood. We examined associations between maternal overweight and obesity severity and risk of cardiovascular diseases in young offspring. These results need to be replicated and possible underlying mechanisms identified.

Offspring of obese mothers have higher rates offsprung cardiovascular events and mortality. All rights reserved. Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. The uterine environment affects organ development, modulating disease susceptibility. In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Substances Biomarkers. Objectives: The aim of this study was to investigate the consequences of maternal overweight on cardiac development in offspring in infants short term and minipigs short and longer term.

Epidemiological studies revealed that maternal obesity is a risk factor maternal obesity and heart disease in the offspring music the development of mental health disorders. The Morris water maze, commonly used hsart assess anxiety-like behavior, exploits a rodents' natural desire to escape from water. Obesity is a common metabolic disorder and is prevalent worldwide [ 1 ]. Lipid accumulation, including cholesterol and phospholipid accumulation, within the glomeruli and proximal tubules is known to be associated with CKD [ 87 ]. In primates, the fetal testes begin producing androgens at the end of the first trimester, with production continuing into the second semester, and a surge at birth Forest et al.

Keywords: cardiac triglycerides; cardiomyopathy; developmental programming; echocardiography; glucose metabolism; positron emission tomography. Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. Keywords: Epigenetics; gestational diabetes; maternal obesity; mitochondria; type 2 diabetes.

  • Leptin regulates appetite-related neuropeptides in the hypothalamus of developing rats without affecting food intake.

  • Abstract Sinceglobal obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. Findings: We identified 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Dec 31,

  • Pre-pregnancy body mass index and gestational weight gain in Thai pregnant women as risks for low birth weight and macrosomia.

  • The uterine environment affects organ development, modulating disease susceptibility. Abstract In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life.

  • Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development.

Swim speed indicates how motivated an animal is to escape, a measure of stress level. Offspring of HFD-fed mothers had increased adiposity, hyperinsulinemia, hyperlipidemia, and insulin resistance. Exposure of the fetus to maternal obesity maternal obesity and heart disease in the offspring music diabetes has in rodent models been suggested to have long-lasting effects on organ development and function, including also neuroendocrine regulation and brain development [ 64 ], through hyperglycemia [ 77 ], oxidative stress [ 7879 ], lipotoxicity [ 8081 ], inflammation [ 828384 ] and the associated hormones insulin and leptin [ 206685 ]. Advanced search. Maternal diabetes and cognitive performance in the offspring: a systematic review and meta-analysis.

A behavioral intervention with diet and physical activity in obese mothers is insufficient to reduce the incidence of fetal macrosomia or to prevent the occurrence of gestational ghe mellitus [ 98 ]. The kidneys of offspring of obese compared with lean mothers examined at Day 20, Week 9 and through to Week 32 showed persistent evidence of inflammation, oxidative stress, and fibrosis. An improvement of diet quality might be an alternative to prevent or lessen obesity-associated adverse health outcomes in offspring. Studies that aim to answer these questions are highly ambitious due to the challenges in recruitment, the number of subjects needed, the length of the follow-up, and the costs; however, they are needed. J Pregnancy. Beneficial and cautionary outcomes of resveratrol supplementation in pregnant nonhuman primates. Maternal prenatal weight gain and autism spectrum disorders.

Methods: In this population-based cohort study, we used data from live singleton births recorded ohesity the Swedish Medical Birth Register. Published by Elsevier Inc. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. Risks of cerebrovascular diseases increased with maternal obesity severity and were partly mediated through asphyxia-related neonatal complications. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined.

Findings: We identified 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Dec 31, While genetic matdrnal and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory. Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes.

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In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Substances Biomarkers. Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. Methods: In this population-based cohort study, we used data from live singleton births recorded in the Swedish Medical Birth Register. In minipigs born to mothers fed a high-fat diet or a normal diet, cardiac development echocardiography, histologyglucose metabolism and perfusion positron emission tomographytriglyceride and glycogen content, and myocardial enzymes regulating metabolism mass spectrometry were determined from birth to adulthood. Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy.

Subsequently, they developed myocardial insulin resistance and glycogen depletion. Longer term effects in minipigs onesity of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function. The uterine environment affects organ development, modulating disease susceptibility. Sinceglobal obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course.

This review critically discusses the current evidence in animal model systems offsprong humans that implicates maternal obesity and diabetes during pregnancy in perturbing diseass epigenome of the next generation, and the consequential impact on growth, organ development and ultimately cardiometabolic disease progression. For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. In fact, maternal obesity and diabetes during pregnancy, which are on the rise, are strongly associated with altered fetal growth and development as well as with lifelong perturbations in metabolic tissues. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory. Keywords: cardiac triglycerides; cardiomyopathy; developmental programming; echocardiography; glucose metabolism; positron emission tomography.

Phase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agent. Rising, R. We confirm that inflammation, oxidative stress, and dyslipidemia are the key mechanisms involved in the relationship between maternal obesity and CKD [ 42—46 ]. Neurochem Res.

Zanoli, P. A systematic review on barriers and facilitators. Young Offspring Alterations Infants born to overweight and obese mothers are more likely to be large for their gestational age and macrosomic [ 46 ]. Search all BMC articles Search.

ALSO READ: National Health And Nutrition Examination Survey Obesity 2010

Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. Ultimately, this knowledge is needed to establish optimal screening, prevention mussic therapeutic approaches for children at risk of cardiometabolic disease development. Methods: Echocardiography was performed in infants born to lean and overweight mothers at birth and at 3, 6, and 12 months of age. DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations. A mounting body of evidence implicates epigenetic mechanisms e.

  • Correlation between maternal and fetal insulin resistance in pregnant women with gestational diabetes mellitus. Regulation of central melanocortin signaling by interleukin-1 beta.

  • Risks of cerebrovascular ans increased with maternal obesity severity and were partly mediated through asphyxia-related neonatal complications. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome.

  • Correspondence to Regina Ensenauer.

These results need to be replicated offsprinh possible underlying mechanisms identified. Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. The uterine environment affects organ development, modulating disease susceptibility. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined.

The sibling-cohort analysis also indicated a positive trend between maternal BMI and cardiovascular disease rates. Methods: Echocardiography was performed in infants born to lean and overweight mothers at birth and at 3, 6, the 12 months of age. Abstract In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. Offspring of obese mothers have higher rates of cardiovascular events and mortality. For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course.

In some case studies, reduced sperm quality disese increased rates of infertility were reported [ 848586 ], whereas others found improvements [ 87 ] or no changes of sperm quality [ 88 ]. Microglia play an active role in obesity-associated cognitive decline. Weight loss further induced a partial normalization of expression levels of a subset of genes belonging to the epigenetic machinery [ 76 ]. These new epigenetic markers—i.

Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations. Longer term effects in minipigs consisted of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function. Publication types Research Support, Non-U.

In minipigs born to mothers fed a high-fat diet or a maternal obesity and heart disease in the offspring music diet, cardiac development echocardiography, histologyglucose metabolism and perfusion positron emission tomographytriglyceride and glycogen content, and myocardial enzymes ovfspring metabolism mass spectrometry were determined from birth to adulthood. Sinceglobal obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. Findings: We identified 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Dec 31, Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring.

Sci Rep. Relationship of prenatal maternal obesity and diabetes to offspring neurodevelopmental and psychiatric disorders: a musix review. Nohr, E. Second, low concentrations of micronutrients, especially those acting as methyl donors, increased the cellular expression of genes that regulate adipogenesis and lipogenesis and altered epigenetic processes [, ]. Mitsuya K.

In addition, this group reported that maternal eating patterns bulimic symptoms, disinhibited eating, hunger, and body dissatisfaction were associated with the onset of secretive eating in children. Catalano P. In preeclampsia patients, both the time and dose of blood pressure control are significantly reduced in those who received resveratrol supplementation [ 77 ]. Increased peripheral insulin levels results in insulin resistance which itself has large effects on the brain and have been associated with depression [ 89909192 ]. CL conceptualized the study, designed the study and led the manuscript writing; LK conducted literature search and wrote the initial draft; XC contributed to manuscript writing; all the authors critically reviewed the manuscript and approved the final manuscript. The offspring of overweight mothers also carried a higher risk of adverse outcomes compared to offspring of mothers with a normal BMI [ 62 ]. Table 2 summarizes some examples of long-term studies using various species to model maternal obesity.

Author contribution S. Obesity and diabetes is a worldwide public health problem among women of reproductive age. The HPA axis regulates the neuroendocrine stress response through circulating cortisol, or in rodent corticosterone. Eur J Epidemiol.

Reprints and Permissions. Importantly, administration of 0. In a study of overweight and obese Spanish women, reduced placental expression of mammalian target of rapamycin and up-regulation of sirtuin 1 and uncoupled protein 2 were demonstrated. Desai M. Archer, J.

Adipocytes secrete inflammatory mediators including chemokines and cytokines which lead to both local and systemic inflammation [ 91 ]. The risk factors of low birth weight infants in the northern part of Thailand. Search Search articles by subject, keyword or author. The identification of risk factors that program mental health disorders in offspring, originating from impairments in the mother's metabolic intrauterine environment, will aid in the development of preventative strategies and therapeutic, dietary interventions. Studies focusing on fertility showed improved fertility rates after modest weight loss of a mean of 6.

Longer term effects in minipigs consisted of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function. DNA methylation and histone modifications in the regulation of these effects and their transmission and heart disease future cisease. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. These results need to be replicated and possible underlying mechanisms identified.

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Publication types Research Support, Non-U. Published by Elsevier Inc. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role dissase early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory. These results need to be replicated and possible underlying mechanisms identified. Objectives: The aim of this study was to investigate the consequences of maternal overweight on cardiac development in offspring in infants short term and minipigs short and longer term. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined.

Intergenerational transmission of the offspring and obesity from parents to their adolescent offspring — the HUNT study. Anxiety disorders in children and adolescents: a review of the past 10 years. However, high-quality studies are sparse. While the association between maternal obesity and offspring neuropsychiatric disorder has been extensively studied, especially for ASD, the influence of maternal diabetes on offspring neuropsychiatric disorders, other than ASD and ADHD [ 111213141516 ], is less well explored. Revised : 20 April Additionally, in adults, a gender bias has been observed in these disorders with the association between obesity and anxiety being stronger in women than men Desai et al.

Study Questions:

Mechanisms underlying overweight development and fetal adipogenic programming through influences of early-life stages are still poorly understood. Mitochondrial dysfunction has been identified in early embryogenesis in obese mothers. Of those, differences in 1. McCurdy et al. The good, the bad, and the ugly of pregnancy nutrients and developmental programming of adult disease.

This review critically discusses the current evidence in animal model systems and humans that implicates maternal obesity and diabetes during pregnancy in perturbing offxpring epigenome of the next generation, and the consequential impact on growth, organ development and ultimately cardiometabolic disease progression. DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations. We examined associations between maternal overweight and obesity severity and risk of cardiovascular diseases in young offspring. The sibling-cohort analysis also indicated a positive trend between maternal BMI and cardiovascular disease rates.

Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. Abstract Sinceglobal obesity has doubled, and the incidence of cardiometabolic diseases such as type 2 diabetes and heart disease is also increasing. For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course. Publication types Research Support, Non-U. Objectives: The aim of this study was to investigate the consequences of maternal overweight on cardiac development in offspring in infants short term and minipigs short and longer term.

Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. The sibling-cohort analysis also indicated a positive trend between maternal BMI and cardiovascular disease rates. Risks of cerebrovascular diseases increased with maternal obesity severity and were partly mediated through asphyxia-related neonatal complications. All rights reserved.

Background

DNA methylation and histone tye in the regulation of these effects and their transmission to future generations. Abstract Objectives: The aim of this study was to investigate the consequences of maternal overweight on cardiac development in offspring in infants short term and minipigs short and longer term. Publication types Research Support, Non-U.

Background: Maternal overweight anf obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study. Ultimately, this knowledge is needed to establish optimal screening, prevention and therapeutic approaches for children at risk of cardiometabolic disease development.

  • In a French cohort study [ 81 ], a restrictive diet and weight loss prior to pregnancy resulted in increased gestational weight gain, which is a known risk factor for large-for-gestational-age birth weight and overweight in children [ 82 ]. A starring role for microglia in brain sex differences.

  • For example, future research requires verification of the mechanistic impact of the epigenetic marks and their persistence over the life course. While genetic susceptibility and adult lifestyle are implicated in these trends, evidence from clinical cohorts, epidemiological studies and animal model experiments support a role for early-life environmental exposures in determining the long-term health of an individual, which has led to the formulation of the Developmental Origins of Health and Disease DOHaD theory.

  • New York, NY: Oxford university press. Importantly, a reduction in the amount of maternal omega-3 fatty acids is associated with increased risk of ADHD and ASD Field,indicating that omega-3 fatty acid supplementation is a promising therapeutic intervention to ameliorate maternal obesity-induced risk of mental health disorders.

  • Our laboratory has developed a nonhuman primate NHP model of diet-induced obesity.

They are believed to be an adaptation mechanism that provides an evolutionary advantage for the subsequent generations. Challier J. Ros et offspringg. The hypothalamus plays a critical role in energy homeostasis by regulating both appetite and energy expenditure. Women who adhered to a Mediterranean style dietary pattern seem to have higher pregnancy rates compared with women eating a Western style diet [ 96 ]. Combined maternal and postnatal high-fat diet leads to metabolic syndrome and is effectively reversed by resveratrol: A multiple-organ study.

This review critically discusses the current evidence in animal model systems and humans that implicates maternal obesity and diabetes during pregnancy in perturbing the epigenome of the next generation, and the consequential umsic on growth, organ development and ultimately cardiometabolic disease progression. These results need to be replicated and possible underlying mechanisms identified. Findings: We identified 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Dec 31, Publication types Research Support, Non-U. In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life.

Pollock1 and Sonia Saad 1. Das S. Brain Mounting evidence from both prenatal and lactational human epidemiologic and animal studies suggests that exposure to maternal obesity and a HFD are associated with neurodevelopmental and psychiatric disorders in offspring.

In the xisease plus maze, rodents have an innate tendency to hide from predators by spending most of their time in the dark and avoiding bright open spaces. Maternal obesity leads to altered nutrient handling [ 38 ], energy modulation [ 39 ], and reduced angiogenesis. Hruby A, Hu FB. One-cell zygote transfer from diabetic to nondiabetic mouse results in congenital malformations and growth retardation in offspring. Severe uncontrolled maternal hyperglycemia induces microsomia and neurodevelopment delay accompanied by apoptosis, cellular survival, and neuroinflammatory deregulation in rat offspring hippocampus. It will detail the known mechanisms of fetal programming, including the role of epigenetic modulation. Childhood consequences of maternal obesity and excessive weight gain during pregnancy.

Journal of Perinatology Maternal body mass index and risk of autism spectrum disorders in offspring: a meta-analysis. Full size image. Adjusted models were subsequently run, adjusting for the above-described confounders.

Srinivasan et al. The impact of gestational diabetes and maternal obesity on the mother and her offspring. Kongubol A, Phupong V. Prenatal Diagn. Geneva: World Health Organization; Epigenetics 8— Drake A.

Introduction

Findings: We identified 2 live singleton infants without congenital malformations in Sweden registered between Jan 1,and Maternxl 31, Subsequently, they developed myocardial insulin resistance and glycogen depletion. Methods: In this population-based cohort study, we used data from live singleton births recorded in the Swedish Medical Birth Register. Keywords: cardiac triglycerides; cardiomyopathy; developmental programming; echocardiography; glucose metabolism; positron emission tomography.

A Swedish cohort including 2, live singleton infants born between and was analyzed. Boocock D. J Clin Endocrinol Metabol. Genetics and epigenetics in obesity. Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring.

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In fact, maternal obesity and diabetes during pregnancy, which are on the rise, are strongly associated with altered fetal growth and development as well as with lifelong perturbations in metabolic tissues. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. Publication types Research Support, Non-U. Longer term effects in minipigs consisted of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function. This review critically discusses the current evidence in animal model systems and humans that implicates maternal obesity and diabetes during pregnancy in perturbing the epigenome of the next generation, and the consequential impact on growth, organ development and ultimately cardiometabolic disease progression. Abstract Background: Maternal overweight and obesity might increase risks of adiposity and cardiovascular and metabolic diseases in offspring.

Rohde et al. Thus, leptin signaling stimulates pro-inflammatory cytokine secretion and influences cortisol release, serotonin and dopaminergic pathways, brain-derived neurotrophic factor BDNF signaling and hippocampal synaptic plasticity [ 93 ]. Olfson, M. Thus, the authors cautioned against the use of resveratrol by pregnant women [ ]. Keywords: metabolic programming, attention deficit hyperactivity disorder, autism spectrum disorders, schizophrenia, mood disorders, eating disorders Citation: Rivera HM, Christiansen KJ and Sullivan EL The role of maternal obesity in the risk of neuropsychiatric disorders.

1. Introduction

Children and adolescents may suffer from eating disorders, such as anorexia nervosa and bulimia nervosa. External link. Adult Offspring Alterations Epidemiological and experimental studies show that maternal obesity is associated with increased susceptibility to hepatic steatosis and inflammation [ 50 ], hypertension and cardiovascular disorders [ 51 ], kidney disease [ 52 ], neurodevelopmental disorders [ 42 ] as well as obesity and insulin resistance [ 53 ] in offspring at different stages of development. Article Google Scholar. Second, a randomized, controlled trial where Gambian women were given micronutrient supplementation, determined that particular candidate genes had altered methylation status as a result of the supplement as measured in cord blood of offspring [ ].

For example, future research requires verification of the mechanistic impact of the epigenetic snd and their persistence over the life course. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. Longer term effects in minipigs consisted of myocardial insulin resistance, enzymatic alterations, and hyperdynamic systolic function. Results: In neonates, maternal overweight, especially in the last trimester, predicted a thicker left ventricular posterior wall at birth 4. Publication types Research Support, Non-U. Published by Elsevier Inc. DNA methylation and histone modifications in the regulation of these effects and their transmission to future generations.

  • The fetal and neonatal hypothalamic—pituitary—adrenal axis.

  • Additionally, this review will address some of the limitations of the DOHaD approach and areas that require further study.

  • Of the bugs that shape us: Maternal obesity, the gut microbiome, and long-term disease risk. Summary of animal research demonstrating that maternal obesity leads to impairments in offspring behavior.

  • Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy.

  • This case control study identified deficient omegafatty acid levels as a nutritional risk factor for ADHD Field,

Pregnancy in type 1 diabetes mellitus: how special are special issues? Maternal obesity also affects adipose tissue development and differentiation during the fetal period [ 4445 ]. Therefore, the future task is the development of a resveratrol formulation with better pharmacokinetic and pharmacodynamic properties. Lagouge M. PubMed Central Google Scholar. The paucity of human studies on substance abuse and addiction should not be interpreted as a lack of effect.

Conclusions: Neonatal changes in cardiac morphology were explained by late-trimester maternal body mass index; myocardial glucose overexposure seen in minipigs can justify early human findings. In addition to immediate implications materna, pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Keywords: Epigenetics; gestational diabetes; maternal obesity; mitochondria; type 2 diabetes.

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