scholarly journals Impact of Maternal Obesity on Fetal Programming of Cardiovascular Disease

Physiology ◽  
2015 ◽  
Vol 30 (3) ◽  
pp. 224-231 ◽  
Author(s):  
Victoria H. J. Roberts ◽  
Antonio E. Frias ◽  
Kevin L. Grove

The in utero environment is a key determinant of long-term health outcomes; poor maternal metabolic state and placental insufficiency are strongly associated with these long-term health risks. Human epidemiological studies link maternal obesity and offspring cardiovascular disease in later life, but mechanistic studies in animal models are limited. Here, we review the literature pertaining to maternal consequences of obesity during pregnancy and the subsequent impact on fetal cardiovascular development.

2019 ◽  
Vol 317 (2) ◽  
pp. H387-H394 ◽  
Author(s):  
Christy-Lynn M. Cooke ◽  
Sandra T. Davidge

Delaying pregnancy, which is on the rise, may increase the risk of cardiovascular disease in both women and their children. The physiological mechanisms that lead to these effects are not fully understood but may involve inadequate adaptations of the maternal cardiovascular system to pregnancy. Indeed, there is abundant evidence in the literature that a fetus developing in a suboptimal in utero environment (such as in pregnancies complicated by fetal growth restriction, preterm birth, and/or preeclampsia) is at an increased risk of cardiovascular disease in adulthood, the developmental origins of health and disease theory. Although women of advanced age are at a significantly increased risk of pregnancy complications, there is limited information as to whether advanced maternal age constitutes an added stressor on the prenatal environment of the fetus, and whether or not this is secondary to impaired cardiovascular function during pregnancy. This review summarizes the current literature available on the impact of advanced maternal age on cardiovascular adaptations to pregnancy and the role of maternal age on long-term health risks for both the mother and offspring.


Author(s):  
Emily S. Barrett ◽  
Susan W. Groth ◽  
Emma V. Preston ◽  
Carolyn Kinkade ◽  
Tamarra James-Todd

Abstract Purpose of Review Pregnancy can be seen as a “stress test” with complications predicting later-life cardiovascular disease risk. Here, we review the growing epidemiological literature evaluating environmental endocrine-disrupting chemical (EDC) exposure in pregnancy in relation to two important cardiovascular disease risk factors, hypertensive disorders of pregnancy and maternal obesity. Recent Findings Overall, evidence of EDC-maternal cardiometabolic associations was mixed. The most consistent associations were observed for phenols and maternal obesity, as well as for perfluoroalkyl substances (PFASs) with hypertensive disorders. Research on polybrominated flame retardants and maternal cardiometabolic outcomes is limited, but suggestive. Summary Although numerous studies evaluated pregnancy outcomes, few evaluated the postpartum period or assessed chemical mixtures. Overall, there is a need to better understand whether pregnancy exposure to these chemicals could contribute to adverse cardiometabolic health outcomes in women, particularly given that cardiovascular disease is the leading cause of death in women.


2013 ◽  
Vol 45 (19) ◽  
pp. 889-900 ◽  
Author(s):  
Alina Maloyan ◽  
Sribalasubashini Muralimanoharan ◽  
Steven Huffman ◽  
Laura A. Cox ◽  
Peter W. Nathanielsz ◽  
...  

Human and animal studies show that suboptimal intrauterine environments lead to fetal programming, predisposing offspring to disease in later life. Maternal obesity has been shown to program offspring for cardiovascular disease (CVD), diabetes, and obesity. MicroRNAs (miRNAs) are small, noncoding RNA molecules that act as key regulators of numerous cellular processes. Compelling evidence links miRNAs to the control of cardiac development and etiology of cardiac pathology; however, little is known about their role in the fetal cardiac response to maternal obesity. Our aim was to sequence and profile the cardiac miRNAs that are dysregulated in the hearts of baboon fetuses born to high fat/high fructose-diet (HFD) fed mothers for comparison with fetal hearts from mothers eating a regular diet. Eighty miRNAs were differentially expressed. Of those, 55 miRNAs were upregulated and 25 downregulated with HFD. Twenty-two miRNAs were mapped to human; 14 of these miRNAs were previously reported to be dysregulated in experimental or human CVD. We used an Ingenuity Pathway Analysis to integrate miRNA profiling and bioinformatics predictions to determine miRNA-regulated processes and genes potentially involved in fetal programming. We found a correlation between miRNA expression and putative gene targets involved in developmental disorders and CVD. Cellular death, growth, and proliferation were the most affected cellular functions in response to maternal obesity. Thus, the current study reveals significant alterations in cardiac miRNA expression in the fetus of obese baboons. The epigenetic modifications caused by adverse prenatal environment may represent one of the mechanisms underlying fetal programming of CVD.


2006 ◽  
Vol 290 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
Barbara T. Alexander

Numerous epidemiological studies suggest an inverse relationship between low birth weight (LBW) and hypertension, an observation now supported by numerous animal studies. The mechanisms linking LBW and hypertension appear to be multifactorial and involve alterations in the normal regulatory systems and renal functions involved in the long-term control of arterial pressure. Recent studies using animal models of fetal programming suggest that programming during fetal life occurs in response to an adverse fetal environment and results in permanent adaptive responses that lead to structural and physiological alterations and the subsequent development of hypertension. This review summarizes the adaptive responses observed in the different models used to induce a suboptimal fetal environment and discusses insights into the mechanisms mediating the fetal programming of hypertension.


2020 ◽  
Vol 91 (5) ◽  
pp. 455-468 ◽  
Author(s):  
Valentina Gallo ◽  
Kim Motley ◽  
Simon P T Kemp ◽  
Saba Mian ◽  
Tara Patel ◽  
...  

IntroductionUnderstanding whether concussion in sport is associated with worsening cognitive function in later life will likely have immediate repercussion on sports concussion prevention and management policy and sporting rules and regulations. This systematic review aims to summarise the evidence on the association between concussion sustained by professional/elite athletes and long-term cognitive impairment.MethodsEmbase, PubMed and Web of Science were used to search for eligible studies. Studies including professional/elite athletes from any sport were considered. Three comparison groups were considered: internal comparison (concussed vs non-concussed athletes within the same sample); between-sport comparison (contact sport athletes vs non-contact sports ones); external comparison (athletes vs samples of the general population or population norms).Results14 studies were included (rugby, American football, ice hockey players, boxers and marital art fighters). The general quality of the evidence was poor. The overall evidence, weighted for type of comparison and study quality, points towards an association between sustaining a sport-related concussion and poorer cognitive function later in life in rugby, American football and boxing, although it is unclear to what extent this is clinically relevant. Data on ice hockey and martial arts were too sparse to allow conclusions to be drawn.ConclusionHigh-quality, appropriately designed and powered epidemiological studies are urgently needed to assess the association between sustaining a sport-related concussion and cognitive impairment later in life. Particular emphasis should be put on the clinical translational value of findings.


Endocrinology ◽  
2021 ◽  
Author(s):  
Niharika Sinha ◽  
Gretchen Lydia Walker ◽  
Aritro Sen

Abstract Altered nutrition or intra-uterine exposure to various adverse conditions during fetal development or earlier in a mother’s life can lead to epigenetic changes in fetal tissues, predisposing those tissues to diseases that manifest when offspring become adults. An example is a maternal obesity associated with gestational diabetes (GDM), where fetal exposure to a hyperglycemic, hyperinsulinemic, and/or hyperlipidemic gestational environment can provoke epigenetic changes that predispose offspring to various diseased conditions later in life. While it is now well established that offspring exposed to GDM have an increased risk of developing obesity, metabolic disorders, and/or cardiovascular disease in adult life, there are limited studies assessing the reproductive health of these offspring. This mini-review discusses the long-term effect of in-utero exposure to GDM-associated adverse prenatal environment on the reproductive health of the offspring. Moreover, using evidence from various animal models and human epidemiological studies this review offers a molecular insight and understanding of how epigenetic reprogramming of genes culminates in reproductive dysfunction and the development of sub/infertility later in adult life.


2020 ◽  
Vol 319 (5) ◽  
pp. R507-R516 ◽  
Author(s):  
Nirajan Shrestha ◽  
Henry C. Ezechukwu ◽  
Olivia J. Holland ◽  
Deanne H. Hryciw

Obesity is an increasing global health epidemic that affects all ages, including women of reproductive age. During pregnancy, maternal obesity is associated with adverse pregnancy outcomes that lead to complications for the mother. In addition, maternal obesity can increase the risk of poor perinatal outcomes for the infant due to altered development. Recent research has investigated the effects of maternal obesity on peripheral organ development and health in later life in offspring. In this review, we have summarized studies that investigated the programming effects of maternal obesity before and during pregnancy on metabolic, cardiovascular, immune, and microbiome perturbations in offspring. Epidemiological studies investigating the effects of maternal obesity on offspring development can be complex due to other copathologies and genetic diversity. Animal studies have provided some insights into the specific mechanisms and pathways involved in programming peripheral disease risk. The effects of maternal obesity during pregnancy on offspring development are often sex specific, with sex-specific changes in placental transport and function suggestive that this organ is likely to play a central role. We believe that this review will assist in facilitating future investigations regarding the underlying mechanisms that link maternal obesity and offspring disease risk in peripheral organs.


2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Kartik Shankar ◽  
Xiaoli Liu ◽  
Amanda Harrell ◽  
Martin J J Ronis ◽  
Thomas M Badger

Reproduction ◽  
2010 ◽  
Vol 140 (3) ◽  
pp. 387-398 ◽  
Author(s):  
Amanda J Drake ◽  
Rebecca M Reynolds

The prevalence of obesity among pregnant women is increasing. In addition to the short-term complications of obesity during pregnancy in both mother and child, it is now recognised that maternal obesity has long-term adverse outcomes for the health of her offspring in later life. Evidence from both animal and human studies indicates that maternal obesity increases the risk for the offspring in developing obesity and altering body composition in child- and adulthood and, additionally, it also has an impact on the offspring's cardiometabolic health with dysregulation of metabolism including glucose/insulin homoeostasis, and development of hypertension and vascular dysfunction. Potential mechanisms include effects on the development and function of adipose tissue, pancreas, muscle, liver, the vasculature and the brain. Further studies are required to elucidate the mechanisms underpinning the programming of disease risk in the offspring as a consequence of maternal obesity. The ultimate aim is to identify potential targets, which may be amenable to prevention or early intervention in order to improve the health of this and future generations.


Sign in / Sign up

Export Citation Format

Share Document