Adverse fetal and neonatal outcomes associated with a life-long high fat diet: role of altered development of the placental vasculature.
Ontology highlight
ABSTRACT:
SUBMITTER: Hayes EK
PROVIDER: S-EPMC3307735 | biostudies-literature | 2012
REPOSITORIES: biostudies-literature
Publications
Adverse fetal and neonatal outcomes associated with a life-long high fat diet: role of altered development of the placental vasculature.
Hayes Emily K EK Lechowicz Anna A Petrik Jim J JJ Storozhuk Yaryna Y Paez-Parent Sabrina S Dai Qin Q Samjoo Imtiaz A IA Mansell Margaret M Gruslin Andree A Holloway Alison C AC Raha Sandeep S
PloS one 20120319 3
Maternal obesity results in a number of obstetrical and fetal complications with both immediate and long-term consequences. The increased prevalence of obesity has resulted in increasing numbers of women of reproductive age in this high-risk group. Since many of these obese women have been subjected to hypercaloric diets from early childhood we have developed a rodent model of life-long maternal obesity to more clearly understand the mechanisms that contribute to adverse pregnancy outcomes in ob ...[more]
Similar Datasets
Project description:Background: Although pregestational obesity has been associated with increased risk of adverse fetal outcome, the mechanisms behind are not known. We aimed to investigate the influence of the maternal metabolic state on fetal outcome in rats exposed to either a high-fat diet (HFD) or a control diet (CD). We also investigated the impact of serum collected from HFD/CD pregnant rats on CD embryonic development in whole-embryo cultures. Material and methods: On gestational day 0, 9, 10, or 20 maternal plasma/serum samples were collected as pregnancies were terminated for the estimations of maternal metabolic state and embryo-fetal development. We measured embryonic gene expression of ROS scavenger enzymes as well as genes involved in inflammation in maternal adipose tissue. Results: In HFD maternal plasma/serum, concentrations of glucose, β-hydroxybutyrate, branched-chain amino acids, and leptin were increased, whereas those of triacylglycerol, cholesterol, and palmitic, oleic, linoleic, and α-linolenic acids were decreased. Gene expression of CuZnSOD, IL-6, IL-10, and resistin was increased in HFD maternal adipose tissue, whereas that of CuZnSOD and MnSOD was decreased in HFD-exposed embryos. HFD caused retention of most fatty acids in the maternal liver as well. Conclusion: HFD alters the maternal metabolic state, increases fetal resorptions in vivo, and increases the rate of fetal/embryonic malformations both in vivo and in vitro. These findings suggest that metabolic disturbances in HFD pregnant rats have profound adverse developmental effects in the offspring.
| S-EPMC6567025 | biostudies-literature
Project description:Maternal metabolic diseases increase offspring risk for low birth weight and cardiometabolic diseases in adulthood. Excess fructose consumption may confer metabolic risks for both women and their offspring. However, the direct consequences of fructose intake per se are unknown. We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the absence of metabolic syndrome and determined the association between maternal serum fructose and placental uric acid levels in humans. In mice, maternal fructose consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose and triglyceride levels. In the placenta, fructose induced de novo uric acid synthesis by activating the activities of the enzymes AMP deaminase and xanthine oxidase. Moreover, the placentas had increased lipids and altered expression of genes that control oxidative stress. Treatment of mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevented placental inefficiency, and improved fetal weights and serum triglycerides. Finally, in 18 women delivering at term, maternal serum fructose levels significantly correlated with placental uric acid levels. These findings suggest that in mice, excess maternal fructose consumption impairs placental function via a xanthine oxidase/uric acid-dependent mechanism, and similar effects may occur in humans.
| S-EPMC4850405 | biostudies-literature
Project description:BackgroundWorldwide, stillbirth is one of the leading causes of death. Altered fetal growth and placental abnormalities are the strongest and most prevalent known risk factors for stillbirth. The aim of this study was to identify patterns of association between placental abnormalities, fetal growth, and stillbirth.Methods and findingsPopulation-based case-control study of all stillbirths and a representative sample of live births in 59 hospitals in 5 geographic areas in the U.S. Fetal growth abnormalities were categorized as small (<10th percentile) and large (>90th percentile) for gestational age at death (stillbirth) or delivery (live birth) using a published algorithm. Placental examination by perinatal pathologists was performed using a standardized protocol. Data were weighted to account for the sampling design. Among 319 singleton stillbirths and 1119 singleton live births at ?24 weeks at death or delivery respectively, 25 placental findings were investigated. Fifteen findings were significantly associated with stillbirth. Ten of the 15 were also associated with fetal growth abnormalities (single umbilical artery; velamentous insertion; terminal villous immaturity; retroplacental hematoma; parenchymal infarction; intraparenchymal thrombus; avascular villi; placental edema; placental weight; ratio birth weight/placental weight) while 5 of the 15 associated with stillbirth were not associated with fetal growth abnormalities (acute chorioamnionitis of placental membranes; acute chorioamionitis of chorionic plate; chorionic plate vascular degenerative changes; perivillous, intervillous fibrin, fibrinoid deposition; fetal vascular thrombi in the chorionic plate). Five patterns were observed: placental findings associated with (1) stillbirth but not fetal growth abnormalities; (2) fetal growth abnormalities in stillbirths only; (3) fetal growth abnormalities in live births only; (4) fetal growth abnormalities in stillbirths and live births in a similar manner; (5) a different pattern of fetal growth abnormalities in stillbirths and live births.ConclusionsThe patterns of association between placental abnormalities, fetal growth, and stillbirth provide insights into the mechanism of impaired placental function and stillbirth. They also suggest implications for clinical care, especially for placental findings amenable to prenatal diagnosis using ultrasound that may be associated with term stillbirths.
| S-EPMC5562325 | biostudies-literature
Project description:STUDY QUESTION:How is endometriosis associated with adverse maternal, fetal and neonatal outcomes of pregnancy? SUMMARY ANSWER:Women with endometriosis are at elevated risk for serious and important adverse maternal (pre-eclampsia, gestational diabetes, placenta praevia and Cesarean section) and fetal or neonatal outcomes (preterm birth, PPROM, small for gestational age, stillbirth and neonatal death). WHAT IS KNOWN ALREADY:A number of studies have shown an association between endometriosis and certain adverse maternal and fetal outcomes, but the results have been conflicting with potential for confounding by the use of assisted reproductive technology. STUDY DESIGN, SIZE, DURATION:A systematic review and meta-analysis of observational studies (1 January 1990-31 December 2017) that evaluated the effect of endometriosis on maternal, fetal and neonatal outcomes was conducted. PARTICIPANTS/MATERIALS, SETTING, METHODS:Studies were considered for inclusion if they were prospective or retrospective cohort or case-control studies; included women greater than 20 weeks gestational age with endometriosis; included a control group of gravid women without endometriosis; and, reported at least one of the outcomes of interest. Each study was reviewed for inclusion, data were extracted and risk of bias was assessed by two independent reviewers. MAIN RESULTS AND THE ROLE OF CHANCE:The search strategy identified 33 studies (sample size, n = 3 280 488) for inclusion. Compared with women without endometriosis, women with endometriosis had higher odds of pre-eclampsia (odds ratio [OR] = 1.18 [1.01-1.39]), gestational hypertension and/or pre-eclampsia (OR = 1.21 [1.05-1.39]), gestational diabetes (OR = 1.26 [1.03-1.55]), gestational cholestasis (OR = 4.87 [1.85-12.83]), placenta praevia (OR = 3.31 [2.37, 4.63]), antepartum hemorrhage (OR = 1.69 [1.38-2.07]), antepartum hospital admissions (OR = 3.18 [2.60-3.87]), malpresentation (OR = 1.71 [1.34, 2.18]), labor dystocia (OR = 1.45 [1.04-2.01]) and cesarean section (OR = 1.86 [1.51-2.29]). Fetuses and neonates of women with endometriosis were also more likely to have preterm premature rupture of membranes (OR = 2.33 [1.39-3.90]), preterm birth (OR = 1.70 [1.40-2.06]), small for gestational age <10th% (OR = 1.28 [1.11-1.49]), NICU admission (OR = 1.39 [1.08-1.78]), stillbirth (OR = 1.29 [1.10, 1.52]) and neonatal death (MOR = 1.78 [1.46-2.16]). Among the subgroup of women who conceived spontaneously, endometriosis was found to be associated with placenta praevia, cesarean section, preterm birth and low birth weight. Among the subgroup of women who conceived with the use of assisted reproductive technology, endometriosis was found to be associated with placenta praevia and preterm birth. LIMITATIONS, REASONS FOR CAUTION:As with any systematic review, the review is limited by the quality of the included studies. The diagnosis for endometriosis and the selection of comparison groups were not uniform across studies. However, the effect of potential misclassification would be bias towards the null hypothesis. WIDER IMPLICATIONS OF THE FINDINGS:The association between endometriosis with the important and serious pregnancy outcomes observed in our meta-analysis, in particular stillbirth and neonatal death, is concerning and warrants further studies to elucidate the mechanisms for the observed findings. STUDY FUNDING/COMPETING INTEREST(S):Dr Shifana Lalani is supported by a Physicians' Services Incorporated Foundation Research Grant, and Dr Innie Chen is supported by a University of Ottawa Clinical Research Chair in Reproductive Population Health and Health Services. Dr Singh declares conflicts of interests with Bayer, Abvie, Allergan and Cooper Surgical. All other authors have no conflicts of interests to declare. REGISTRATION NUMBER:PROSPERO CRD42015013911.
| S-EPMC6145420 | biostudies-literature
Project description:ObjectiveTo analyse outcomes in different forms of persistent fetal vasculature (PFV).Methods and analysisRetrospective cohort study at a university-based practice of children presenting with PFV between 2011 and 2020. Exclusion criteria was surgical management outside of our institution and follow-up less than 1 month. Wilcoxon and Student's t-tests were used for statistical analysis.ResultsForty-six eyes of 45 patients presented with PFV at 16.7±31.3 (median 2.8) months old with 32.6±29.8 (median 22.5) months of follow-up. Types of PFV included: mild combined anterior-posterior (23 eyes, 50%), severe combined anterior-posterior (18 eyes, 39%), severe anterior (3 eyes, 7%), mild anterior (1 eye, 2%) and posterior (1 eye, 2%). Thirty-two eyes (70%) underwent PFV surgical correction; lensectomy (13 mild combined), vitrectomy (3 mild combined), sequential lensectomy then vitrectomy (3 severe combined), combined lensectomy-vitrectomy (11 severe anterior or severe combined), laser retinopexy (1 mild combined). Five eyes required additional vitrectomy surgery for retinal detachment, fold or cyclitic membrane. Nine eyes developed glaucoma, six requiring Intraocular pressure (IOP)-lowering surgery. At final follow-up, 32 eyes had at least form vision and 6 eyes were aversive to light. Eight eyes, all which were severe combined, and four that did not undergo PFV surgery, were unable to detect light due to phthisis bulbi (7) and optic nerve hypoplasia (1).ConclusionsClassification of PFV is important in determining surgical approach with severe cases often requiring both lensectomy and vitrectomy for optimal anatomic and functional outcomes.
| S-EPMC8094357 | biostudies-literature
Project description:Placental abruption (early separation of the placenta) is associated with preterm birth and perinatal mortality, but associations with other neonatal morbidities remain understudied. We examined the association between abruption and newborn outcomes. We analyzed 223,341 singleton deliveries from the Consortium on Safe Labor study, a retrospective, multisite, observational study (2002-2008) of electronic medical records in the United States. Adjusted relative risks, incidence rate ratios, and 99% confidence intervals were estimated. Direct effects attributable to abruption were examined by conditioning on intermediates (preterm birth and small for gestational age) with sensitivity analyses. Incidence of abruption was 1.6% (n = 3,619). Abruption was associated with an elevated risk of newborn resuscitation (relative risk (RR) = 1.5, 99% confidence interval (CI): 1.5, 1.6), apnea (RR = 5.8, 99% CI: 5.1, 6.5), asphyxia (RR = 8.5, 99% CI: 5.7, 11.3), respiratory distress syndrome (RR = 6.5, 99% CI: 5.9, 7.1), neonatal intensive care unit admission (RR = 3.4, 99% CI: 3.2, 3.6), longer intensive care length of stay (incidence rate ratio = 2.0, 99% CI: 1.9, 2.2), stillbirth (RR = 6.3, 99% CI: 4.7, 7.9), and neonatal mortality (RR = 7.6, 99% CI: 5.2, 10.1). In sensitivity analyses, there was a direct effect of abruption associated with increased neonatal risks. These findings expand our knowledge of the association between abruption and perinatal and neonatal outcomes.
| S-EPMC5860509 | biostudies-literature
Project description:The mechanistic basis of the proposed relationship between maternal cardiac output and neonatal complications in pregnant women with heart disease has not been well elucidated.Pregnant women with cardiac disease and healthy pregnant women (controls) were prospectively followed with maternal echocardiography and obstetrical ultrasound scans at baseline, third trimester, and postpartum. Fetal/neonatal complications (death, small-for-gestational-age or low birthweight, prematurity, respiratory distress syndrome, or intraventricular hemorrhage) comprised the primary study outcome. One hundred and twenty-seven women with cardiac disease and 45 healthy controls were enrolled. Neonatal events occurred in 28 pregnancies and were more frequent in the heart disease group as compared with controls (n=26/127 or 21% versus n=2/45 or 4%; P=0.01). Multiple complications in an infant were counted as a single outcome event. Neonatal complications in the heart disease group were small-for-gestational-age/low birthweight (n=18), prematurity (n=14), and intraventricular hemorrhage/respiratory distress syndrome (n=5). Preexisting obstetric risk factors (P=0.003), maternal cardiac output decline from baseline to third trimester (P=0.017), and third trimester umbilical artery Doppler abnormalities (P<0.001) independently predicted neonatal complications and were incorporated into a novel risk index in which 0, 1, and >1 predictor corresponded to expected complication rates of 5%, 30%, and 76%, respectively.Decline in maternal cardiac output during pregnancy and abnormal umbilical artery Doppler flows independently predict neonatal complications. These findings will enhance the identification of higher risk pregnancies that would benefit from close antenatal surveillance.
| S-EPMC4845210 | biostudies-other
Project description:The typical US diet has >30% calories from fat; yet, typical laboratory diets contain 17% calories from fat. This disparity could confound the clinical relevance of findings in cerebral ischemia models. We compared outcomes after neonatal brain injury in offspring of rat dams fed standard low-fat chow (17% fat calories) or a higher fat diet (34% fat calories) from day 7 of pregnancy. On postnatal day 7, hypoxic-ischemic injury was induced by right carotid ligation, followed by 60, 75 or 90 min 8% oxygen exposure. Sensorimotor function, brain damage, and serum and brain fatty acid content were compared 1 to 4 weeks later. All lesioned animals developed left forepaw placing deficits; scores were worse in the high-fat groups (p < 0.0001, ANOVA). Similarly, reductions in left forepaw grip strength were more pronounced in the high-fat groups. Severity of right hemisphere damage increased with hypoxia-ischemia duration but did not differ between diet groups. Serum and brain docosahexaenoic acid fatty acid fractions were lower in high-fat progeny (p < 0.05, ANOVA). We speculate that the high-fat diet disrupted docosahexaenoic acid-dependent recovery mechanisms. These findings have significant implications both for refinement of neonatal brain injury models and for understanding the impact of maternal diet on neonatal neuroplasticity.
| S-EPMC5363747 | biostudies-literature
Project description:BackgroundSickle cell disease in pregnancy is associated with high maternal and fetal mortality. However, studies reporting pregnancy, fetal, and neonatal outcomes in women with sickle cell disease are extremely limited.ObjectivesThe objectives of the study are to determine whether women with sickle cell disease have a greater risk of adverse pregnancy, fetal, and neonatal outcomes than women without sickle cell disease and identify the predictors of adverse pregnancy, fetal, and neonatal outcomes in women with sickle cell disease.DesignA retrospective pair-matched case-control study was conducted to compare 171 pregnant women with sickle cell disease to 171 pregnant women without sickle cell disease in Muscat, Sultanate of Oman.MethodsAll pregnant Omani women with sickle cell disease who delivered between January 2015 and August 2021 at Sultan Qaboos University Hospital and Royal Hospital, who were either primipara or multipara and who had a gestational age of 24-42 weeks, were included as patients, whereas women who had no sickle cell disease or any comorbidity during pregnancy, who delivered within the same timeframe and at the same hospitals, were recruited as controls. The data were retrieved from electronic medical records and delivery registry books between January 2015 and August 2021.ResultsWomen with sickle cell disease who had severe anemia had increased odds of (χ2 = 58.56, p < 0.001) having adverse pregnancy outcomes. Women with sickle cell disease had 21.97% higher odds of delivering a baby with intrauterine growth retardation (χ2 = 17.80, unadjusted odds ratio = 2.91-166.13, p < 0.001). Newborns born to women with sickle cell disease had 3.93% greater odds of being admitted to the neonatal intensive care unit (χ2 = 16.80, unadjusted odds ratio = 1.97-7.84, p < 0.001). In addition, the children born to women with sickle cell disease had 10.90% higher odds of being born with low birth weight (χ2 = 56.92, unadjusted odds ratio = 5.36-22.16, p < 0.001). Hemoglobin level (odds ratio = 0.17, p < 0.001, 95% confidence interval = 0.10-3.0), past medical history (odds ratio = 7.95, p < 0.001, 95% confidence interval = 2.39-26.43), past surgical history (odds ratio = 17.69, p < 0.001, 95% confidence interval = 3.41-91.76), and preterm delivery (odds ratio = 9.48, p = 0.005, 95% confidence interval = 1.95-46.23) were identified as predictors of adverse pregnancy, fetal, and neonatal outcomes in women with sickle cell disease.ConclusionAs pregnant women with sickle cell disease are at increased risk for pregnancy, fetal, and neonatal adverse outcomes; improved antenatal surveillance and management may improve the outcomes.
| S-EPMC10838028 | biostudies-literature
Project description:Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a disease that causes thrombocytopenia and a risk of bleeding in the (unborn) child that result from maternal alloantibodies directed against fetal, paternally inherited, human platelet antigens (HPA). It is hypothesized that these alloantibodies can also bind to the placenta, causing placental damage. This study aims to explore signs of antibody-mediated placental damage in FNAIT. We performed a retrospective study that included pregnant women, their newborns, and placentas. It comprised 23 FNAIT cases, of which nine were newly diagnosed (14 samples) and 14 were antenatally treated with intravenous immune globulins (IVIg) (21 samples), and 20 controls, of which 10 had anti-HLA-class I antibodies. Clinical information was collected from medical records. Placental samples were stained for complement activation markers (C1q, C4d, SC5b-9, and mannose-binding lectin) using immunohistochemistry. Histopathology was examined according to the Amsterdam criteria. A higher degree of C4d deposition was present in the newly diagnosed FNAIT cases (10/14 samples), as compared to the IVIg-treated FNAIT cases (2/21 samples, p = 0.002) and anti-HLA-negative controls (3/20 samples, p = 0.006). A histopathological examination showed delayed maturation in four (44%) placentas in the newly diagnosed FNAIT cases, five (36%) in the IVIg-treated FNAIT cases, and one in the controls (NS). C4d deposition at the syncytiotrophoblast was present in combination with low-grade villitis of unknown etiology in three newly diagnosed FNAIT cases that were born SGA. We conclude that a higher degree of classical pathway-induced complement activation is present in placentas from pregnancies with untreated FNAIT. This may affect placental function and fetal growth.
| S-EPMC8267834 | biostudies-literature