scholarly journals Effects of maternal obesity on placental function and fetal development

Reproduction ◽  
2017 ◽  
Vol 153 (3) ◽  
pp. R97-R108 ◽  
Author(s):  
Kristy R Howell ◽  
Theresa L Powell
Keyword(s):  
Fetal Development ◽  
Maternal Obesity ◽  
Critical Role ◽  
Obese Women ◽  
Necrosis Factor Alpha ◽  
Nutrient Delivery ◽  
Placental Function ◽  
Metabolic Hormones ◽  
Increased Risk

Obesity has reached epidemic proportions, and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, pre-term birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines, i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction including insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers.

scholarly journals The impact of gestational diabetes and maternal obesity on the mother and her offspring

2010 ◽  
Vol 1 (4) ◽  
pp. 208-215 ◽  
Author(s):  
P. M. Catalano
Keyword(s):  
Insulin Resistance ◽  
Gestational Diabetes ◽  
Glucose Intolerance ◽  
Maternal Obesity ◽  
Insulin Response ◽  
Obese Women ◽  
Increased Risk ◽  
Short And Long Term ◽  
The Impact

Thein uteromaternal metabolic environment is important relative to both short and long term development of the offspring. Although poor fetal growth remains a significant factor relative to long-term outcome, fetal overgrowth is assuming greater importance because of the increase in obesity in the world’s populations. Maternal obesity and gestational diabetes are the most common metabolic complications of pregnancy related to fetal overgrowth and more specifically adiposity.Women with gestational diabetes have increased insulin resistance and inadequate insulin response compared with weight-matched controls. Gestational diabetes increases the risk of maternal hypertensive disease (preeclampsia) as well as cesarean delivery. At birth the neonate has increased adiposity and is at risk for birth injury. Multiple studies have reported that children of women with gestational diabetes have a greater prevalence childhood obesity and glucose intolerance; even at glucose concentrations less than currently used to define gestational diabetes, compared with normoglycemic women.Obese women also have increased insulin resistance, insulin response and inflammatory cytokines compared with average weight women both before and during pregnancy. They too are at increased risk for the metabolic syndrome-like disorders during pregnancy that is hypertension, hyperlipidemia, glucose intolerance and coagulation disorders. Analogous to women with gestational diabetes, neonates of obese women are heavier at delivery because of increased fat and not lean body mass. Similarly, these children have an increased risk of childhood adiposity and metabolic dysregulation. Hence, the preconceptional and perinatal period offers a unique opportunity to modify both short and long term risks for both the woman and her offspring.

scholarly journals Placental function in maternal obesity

2020 ◽  
Vol 134 (8) ◽  
pp. 961-984 ◽  
Author(s):  
Amy C. Kelly ◽  
Theresa L. Powell ◽  
Thomas Jansson
Keyword(s):  
Pregnant Women ◽  
Maternal Obesity ◽  
Normal Weight ◽  
Adverse Outcomes ◽  
Obese Women ◽  
Long Term Outcomes ◽  
Placental Function ◽  
High Insulin ◽  
Short And Long Term

Abstract Maternal obesity is associated with pregnancy complications and increases the risk for the infant to develop obesity, diabetes and cardiovascular disease later in life. However, the mechanisms linking the maternal obesogenic environment to adverse short- and long-term outcomes remain poorly understood. As compared with pregnant women with normal BMI, women entering pregnancy obese have more pronounced insulin resistance, higher circulating plasma insulin, leptin, IGF-1, lipids and possibly proinflammatory cytokines and lower plasma adiponectin. Importantly, the changes in maternal levels of nutrients, growth factors and hormones in maternal obesity modulate placental function. For example, high insulin, leptin, IGF-1 and low adiponectin in obese pregnant women activate mTOR signaling in the placenta, promoting protein synthesis, mitochondrial function and nutrient transport. These changes are believed to increase fetal nutrient supply and contribute to fetal overgrowth and/or adiposity in offspring, which increases the risk to develop disease later in life. However, the majority of obese women give birth to normal weight infants and these pregnancies are also associated with activation of inflammatory signaling pathways, oxidative stress, decreased oxidative phosphorylation and lipid accumulation in the placenta. Recent bioinformatics approaches have expanded our understanding of how maternal obesity affects the placenta; however, the link between changes in placental function and adverse outcomes in obese women giving birth to normal sized infants is unclear. Interventions that specifically target placental function, such as activation of placental adiponectin receptors, may prevent the transmission of metabolic disease from obese women to the next generation.

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

Obesity and oocyte quality: Significant implications for ART and Emerging mechanistic insights

2021 ◽  
Author(s):  
Macarena B Gonzalez ◽  
Rebecca L Robker ◽  
Ryan D Rose
Keyword(s):  
Pregnancy Complications ◽  
Maternal Obesity ◽  
Ovarian Function ◽  
Polycystic Ovary ◽  
Live Birth Rate ◽  
Oocyte Quality ◽  
Reproductive Age ◽  
Developmental Competence ◽  
Obese Women ◽  
Increased Risk

Abstract The prevalence of obesity in adults worldwide, and specifically in women of reproductive age, is concerning given the risks to fertility posed by the increased risk of type 2 diabetes, metabolic syndrome and other non-communicable diseases. Obesity has a multi-systemic impact in female physiology that is characterized by the presence of oxidative stress, lipotoxicity, and the activation of pro-inflammatory pathways, inducing tissue-specific insulin resistance and ultimately conducive to abnormal ovarian function. A higher body mass is linked to Polycystic Ovary Syndrome, dysregulated menstrual cycles, anovulation, and longer time to pregnancy, even in ovulatory women. In the context of ART, compared to women of normal BMI, obese women have worse outcomes in every step of their journey, resulting in reduced success measured as live birth rate. Even after pregnancy is achieved, obese women have a higher chance of miscarriage, gestational diabetes, pregnancy complications, birth defects, and most worryingly, a higher risk of stillbirth and neonatal death. The potential for compounding effects of ART on pregnancy complications and infant morbidities in obese women has not been studied. There is still much debate in the field on whether these poorer outcomes are mainly driven by defects in oocyte quality, abnormal embryo development or an unaccommodating uterine environment, however the clinical evidence to date suggests a combination of all three are responsible. Animal models of maternal obesity shed light on the mechanisms underlaying the effects of obesity on the peri-conception environment, with recent findings pointing to lipotoxicity in the ovarian environment as a key driver of defects in oocytes that have not only reduced developmental competence but long-lasting effects in offspring health.

scholarly journals NURR1 Alterations in Perinatal Stress: A First Step towards Late-Onset Diseases? A Narrative Review

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 584
Author(s):  
Laura Bordoni ◽  
Irene Petracci ◽  
Jean Calleja-Agius ◽  
Joan G. Lalor ◽  
Rosita Gabbianelli
Keyword(s):  
Maternal Obesity ◽  
Late Onset ◽  
Critical Role ◽  
Perinatal Period ◽  
Narrative Review ◽  
Low Grade ◽  
Vaginal Infections ◽  
Increased Risk ◽  
Gestational Tissues ◽  
Early Life Events

Perinatal life represents a delicate phase of development where stimuli of all sorts, coming to or from the mother, can influence the programming of the future baby’s health. These stimuli may have consequences that persist throughout adulthood. Nuclear receptor related 1 protein (NURR1), a transcription factor with a critical role in the development of the dopaminergic neurons in the midbrain, mediates the response to stressful environmental stimuli in the perinatal period. During pregnancy, low-grade inflammation triggered by maternal obesity, hyperinsulinemia or vaginal infections alters NURR1 expression in human gestational tissues. A similar scenario is triggered by exposure to neurotoxic compounds, which are associated with NURR1 epigenetic deregulation in the offspring, with potential intergenerational effects. Since these alterations have been associated with an increased risk of developing late-onset diseases in children, NURR1, alone, or in combination with other molecular markers, has been proposed as a new prognostic tool and a potential therapeutic target for several pathological conditions. This narrative review describes perinatal stress associated with NURR1 gene deregulation, which is proposed here as a mediator of late-onset consequences of early life events.

Maternal Obesity and Risk for Birth Defects

PEDIATRICS ◽  
2003 ◽  
Vol 111 (Supplement_1) ◽  
pp. 1152-1158 ◽  
Author(s):  
Margaret L. Watkins ◽  
Sonja A. Rasmussen ◽  
Margaret A. Honein ◽  
Lorenzo D. Botto ◽  
Cynthia A. Moore
Keyword(s):  
Spina Bifida ◽  
Birth Defects ◽  
Maternal Obesity ◽  
Heart Defects ◽  
Average Weight ◽  
Maternal Body Mass Index ◽  
Healthy Weight ◽  
Obese Women ◽  
Overweight Women ◽  
Increased Risk

Objective. Several studies have shown an increased risk for neural tube defects associated with prepregnancy maternal obesity. Because few recent studies have examined the relation between maternal prepregnancy obesity and overweight and other birth defects, we explored the relation for several birth defects and compared our findings with those of previous studies. Methods. We conducted a population-based case-control study of several selected major birth defects using data from the Atlanta Birth Defects Risk Factor Surveillance Study. Mothers who delivered an infant with and without selected birth defects in a 5-county metropolitan Atlanta area between January 1993 and August 1997 were interviewed. Maternal body mass index (BMI) was calculated from self-reported maternal prepregnancy weight and height. Women with known preexisting diabetes were excluded. The risks for obese women (BMI ≥30) and overweight women (BMI 25.0–29.9) were compared with those for average-weight women (BMI 18.5–24.9). Results. Obese women were more likely than average-weight women to have an infant with spina bifida (unadjusted odds ratio [OR]: 3.5; 95% confidence interval [CI]: 1.2–10.3), omphalocele (OR: 3.3; 95% CI: 1.0–10.3), heart defects (OR: 2.0; 95% CI: 1.2–3.4), and multiple anomalies (OR: 2.0; 95% CI: 1.0–3.8). Overweight women were more likely than average-weight women to have infants with heart defects (OR: 2.0; 95% CI: 1.2–3.1) and multiple anomalies (OR: 1.9; 95% CI: 1.1–3.4). Conclusions. Our study confirmed the previously established association between spina bifida and prepregnancy maternal obesity and found an association for omphalocele, heart defects, and multiple anomalies among infants of obese women. We also found an association between heart defects and multiple anomalies and being overweight before pregnancy. A higher risk for some birth defects is yet another adverse pregnancy outcome associated with maternal obesity. Obesity prevention efforts are needed to increase the number of women who are of healthy weight before pregnancy.

The impact of parity and maternal obesity on the fetal outcomes of a non-selected Lower Saxony population

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Lars Brodowski ◽  
Niels Rochow ◽  
Efrah I. Yousuf ◽  
Fabian Kohls ◽  
Constantin S. von Kaisenberg ◽  
...  
Keyword(s):  
Maternal Obesity ◽  
Fetal Distress ◽  
Maternal Body Mass Index ◽  
Obese Women ◽  
Lower Saxony ◽  
Fetal Outcomes ◽  
Increased Risk ◽  
Longitudinal Position ◽  
The Impact ◽  
Maternal Bmi

Abstract Objectives Maternal obesity during pregnancy is associated with adverse intrauterine events and fetal outcomes and may increase the risk of obesity and metabolic disease development in offspring. Higher parity, regardless of socioeconomic status, is associated with increased maternal body mass index (BMI). In this study, we examined the relationship between parity, maternal obesity, and fetal outcomes in a large sample of mother-neonate pairs from Lower Saxony, Germany. Methods This retrospective cohort study examined pseudonymized data of a non-selected singleton cohort from Lower Saxony’s statewide quality assurance initiative. 448,963 cases were included. Newborn outcomes were assessed in relation to maternal BMI and parity. Results Maternal obesity was associated with an increased risk of placental insufficiency, chorioamnionitis, and fetal distress while giving birth. This effect was present across all parity groups. Fetal presentation did not differ between BMI groups, except for the increased risk of high longitudinal position and shoulder dystocia in obese women. Maternal obesity was also associated with an increased risk of premature birth, low arterial cord blood pH and low 5-min APGAR scores. Conclusions Maternal obesity increases the risk of adverse neonatal outcomes. There is a positive correlation between parity and increased maternal BMI. Weight-dependent fetal risk factors increase with parity, while parity-dependent outcomes occur less frequently in multipara. Prevention and intervention programs for women planning to become pregnant can be promising measures to reduce pregnancy and birth complications.

scholarly journals A comparative study of the effect of body mass index on pregnancy outcomes in normal and overweight women

2017 ◽  
Vol 6 (4) ◽  
pp. 1550
Author(s):  
Seeniammal P. ◽  
Chellamma V. K. ◽  
Umadevi N.
Keyword(s):  
Comparative Study ◽  
Maternal Obesity ◽  
Gestational Hypertension ◽  
Fetal Outcome ◽  
Overweight And Obesity ◽  
Health Concern ◽  
Accurate Information ◽  
Obese Women ◽  
Increased Risk ◽  
Maternal Overweight

Background: Maternal obesity has been reported as a risk factor for various antepartum, intrapartum, postpartum and neonatal complications. Increasing rates of overweight among pregnant women are a significant public health concern with various implications for prenatal care and supervision of delivery. Therefore, the present study is to determine the adverse materno-fetal outcome in primigravid overweight and obese women delivering singleton babies.Methods: A prospective comparative study was conducted for a year at IMCH, Medical College, Calicut. Primigravid women with a singleton uncomplicated pregnancy with cephalic presentation at ≥37 weeks of gestation with accurate information regarding height and weight recorded at the booking visit were included in the study. Comparisons were made between 100 women with BMI >25 and 200 women with BMI 18.5-24.9. Statistical analysis was done using SPSS version 16.0. Data was analysed by Pearson Chi square test and Fisher’s exact test.Results: Overweight mothers are at increased risk quoted as relative risk (RR) and 95% confidence intervals (CI) of adverse materno-fetal outcomes. Gestational hypertension RR 2.39 (CI 1.65-3.47), Gestational diabetes RR 2.67(CI 0.95-7.48), induction of labour RR 2.35 (CI 1.4-3.95), Cesarean section RR 5.73 (CI 3.76-8.73), macrosomia RR 14 (CI 1.75-112.23), NICU admissions RR 4.51(CI 2.61-7.84),perineal lacerations RR 4.72 (CI 1.15-20.4), wound infection RR 2.97 (CI 1.06-8.41), and prolonged hospital stay.Conclusions: It is clearly evident from the study that maternal overweight and obesity is associated with adverse materno-fetal outcome.

scholarly journals Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women

2008 ◽  
Vol 100 (5) ◽  
pp. 947-952 ◽  
Author(s):  
Michael M. Swarbrick ◽  
Kimber L. Stanhope ◽  
Sharon S. Elliott ◽  
James L. Graham ◽  
Ronald M. Krauss ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Human Subjects ◽  
Area Under The Curve ◽  
Metabolic Effects ◽  
Obese Women ◽  
Complex Carbohydrate ◽  
Sweetened Beverages ◽  
The Metabolic Syndrome ◽  
Increased Risk

Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26·8–33·3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0·0002,P = 0·007 andP = 0·013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0·04). Fructose also increased fasting apoB concentrations by 19 % (P = 0·043v.baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.

scholarly journals NLRP3-Inflammasome Inhibition during Respiratory Virus Infection Abrogates Lung Immunopathology and Long-Term Airway Disease Development

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 692
Author(s):  
Carrie-Anne Malinczak ◽  
Charles F. Schuler ◽  
Angela J. Duran ◽  
Andrew J. Rasky ◽  
Mohamed M. Mire ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Severe Disease ◽  
Critical Role ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Increased Risk ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) infects most infants by two years of age. It can cause severe disease leading to an increased risk of developing asthma later in life. Previously, our group has shown that RSV infection in mice and infants promotes IL-1β production. Here, we characterized the role of NLRP3-Inflammasome activation during RSV infection in adult mice and neonates. We observed that the inhibition of NLRP3 activation using the small molecule inhibitor, MCC950, or in genetically modified NLRP3 knockout (Nlrp3−/−) mice during in vivo RSV infection led to decreased lung immunopathology along with a reduced expression of the mucus-associated genes and reduced production of innate cytokines (IL-1β, IL-33 and CCL2) linked to severe RSV disease while leading to significant increases in IFN-β. NLRP3-inflammasome inhibition or deletion diminished Th2 cytokines and inflammatory cell infiltration into the lungs. Furthermore, NLRP3 inhibition or deletion during early-life RSV infection led to reducing viral-exacerbated allergic response in a mouse model of RSV-induced allergy exacerbation. Here, we demonstrated the critical role of NLRP3-inflammasome activation in RSV immunopathology and the related long-term airway alteration. Moreover, these findings suggest the NLRP3-inflammasome as a potential therapeutic target to attenuate severe RSV disease and limit childhood asthma development.

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