scholarly journals Placental weight mediates the effects of prenatal factors on fetal growth: the extent differs by preterm status

Obesity ◽  
2013 ◽  
Vol 21 (3) ◽  
pp. 609-620 ◽  
Author(s):  
Fengxiu Ouyang ◽  
Margaret Parker ◽  
Sandra Cerda ◽  
Colleen Pearson ◽  
Lingling Fu ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Placental Weight ◽  
Prenatal Factors

scholarly journals Placental Weight Mediates the Effects of Prenatal Factors on Fetal Growth: The Extent Differs by Preterm Status

Obesity ◽  
2012 ◽  
Author(s):  
Fengxiu Ouyang ◽  
Margaret Parker ◽  
Sandra Cerda ◽  
Colleen Pearson ◽  
Lingling Fu ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Placental Weight ◽  
Prenatal Factors

Maternal Marijuana Exposure, Feto-Placental Weight Ratio, and Placental Histology

2020 ◽  
Author(s):  
Torri D. Metz ◽  
Amanda A. Allshouse ◽  
Halit Pinar ◽  
Michael Varner ◽  
Marcela C. Smid ◽  
...  
Keyword(s):  
Tobacco Use ◽  
Fetal Growth ◽  
Statistical Significance ◽  
Weight Ratio ◽  
Marijuana Use ◽  
Placental Weight ◽  
Self Report ◽  
Serum Cotinine ◽  
Fetal Sex ◽  
Live Births

Objective Marijuana use is associated with placenta-mediated adverse pregnancy outcomes including fetal growth restriction, but the mechanism remains uncertain. The objective was to evaluate the association between maternal marijuana use and the feto-placental weight ratio (FPR). Secondarily, we aimed to compare placental histology of women who used marijuana to those who did not. Study Design This was a secondary analysis of singleton pregnancies enrolled in a multicenter and case–control stillbirth study. Prior marijuana use was detected by electronic medical record abstraction or cord homogenate positive for 11-nor-delta-9-tetrahydrocannabinol-9-carboxylic acid. Prior tobacco use was detected by self-report or presence of maternal serum cotinine. Stillbirths and live births were considered separately. The primary outcome was FPR. Association of marijuana use with FPR was estimated with multivariable linear modeling adjusted for fetal sex, preterm birth, and tobacco use. Comparisons between groups for placental histology were made using Chi-square and stratified by live birth and stillbirth, term and preterm deliveries, and fetal sex. Results Of 1,027 participants, 224 were stillbirths and 803 were live births. Overall, 41 (4%) women used marijuana during the pregnancy. The FPR ratio was lower among exposed offspring but reached statistical significance only for term stillbirths (mean 6.84 with marijuana use vs. mean 7.8 without use, p < 0.001). In multivariable modeling, marijuana use was not significantly associated with FPR (p = 0.09). There were no differences in histologic placental features among those with and without marijuana use overall or in stratified analyses. Conclusion Exposure to marijuana may not be associated with FPR. Similarly, there were no placental histologic features associated with marijuana exposure. Further study of the influence of maternal marijuana use on placental development and function is warranted to better understand the association between prenatal marijuana use and poor fetal growth. Key Points

scholarly journals Leptin Concentrations in Maternal and Umbilical Cord Blood in Relation to Maternal Weight, Birth Weight and Weight of the Placenta

1970 ◽  
Vol 23 (1) ◽  
pp. 3-7 ◽  
Author(s):  
S Ishrat ◽  
MW Rahman ◽  
MR Rahman ◽  
MZ Hussain ◽  
S Jahan
Keyword(s):  
Birth Weight ◽  
Cord Blood ◽  
Fetal Growth ◽  
Leptin Receptor ◽  
Venous Blood ◽  
The Body ◽  
Placental Weight ◽  
Enzyme Linked Immunosorbent Assay ◽  
Maternal Weight ◽  
Serum Leptin

Objective: Leptin is a hormone which regulates adipose tissue mass of the body. Substantial increase of leptin during pregnancy and detection of leptin and leptin receptor in placenta have led to the speculation that leptin is a gestational hormone with a possible role in regulation of fetal growth. The study was done to find out whether maternal and cord blood leptin correlate with birthweight and weight of the placenta. Materials and methods: A prospective cross sectional study was undertaken in the Department of Obsterics and Gynecology, Bangabandhu Sheikh Mujib Medical University from January 2005 to June 2005. The study was carried out on 39 pairs of mothers and newborns. Maternal venous blood was sampled just before delivery. Cord blood was obtained, birth weight and placental weight measurements were taken just after delivery of the baby. Serum leptin levels were measured by enzyme linked immunosorbent assay. Results: Maternal serum leptin was 24.50 ng/ml (range- 13.15-45.60 ng/ml) and cord serum leptin was 6.50 ng/ml (range- 2.02-12.30 ng/ml). There was no correlation between maternal leptin and birth weight or between maternal leptin and placental weight. Cord leptin was significantly correlated with birth weight but not with placental weight. There was no correlation between maternal and cord blood leptin. There was no significant gender differences in cord blood leptin concentrations. Conclusions: There may be an important role of leptin in regulation of fetal growth and development. Placenta may not be a major source of leptin in maternal and feto-placental circulation. Maternal leptin cannot be a reliable marker of fetal growth. Keywords: Serum leptin, birth weight, placental weight   doi: 10.3329/bjog.v23i1.3049 Bangladesh J Obstet Gynaecol, 2008; Vol. 23(1) : 3-7

scholarly journals Fetal growth and ratio of placental weight to birth weight.

BMJ ◽  
1992 ◽  
Vol 304 (6827) ◽  
pp. 638-638 ◽  
Author(s):  
R. De Courcy-Wheeler ◽  
C. Wolfe
Keyword(s):  
Birth Weight ◽  
Fetal Growth ◽  
Placental Weight

scholarly journals 273.Insulin-like growth factor treatment of pregnant guinea pigs during early pregnancy promotes fetal growth

2004 ◽  
Vol 16 (9) ◽  
pp. 273
Author(s):  
A. N. Sferruzzi-Perri ◽  
J. A. Owens ◽  
J. S. Robinson ◽  
C. T. Roberts
Keyword(s):  
Growth Factor ◽  
Fetal Growth ◽  
Early Pregnancy ◽  
Guinea Pigs ◽  
Placental Weight ◽  
Fetal Weight ◽  
Abdominal Circumference ◽  
Insulin Like Growth Factor ◽  
Crown Rump Length ◽  
Igf I

Insulin-like growth factor (IGF)-II is an important regulator of growth in many tissues and is abundantly expressed in the placenta during pregnancy. Gene ablation studies performed in mice have shown that IGF-II deficiency results in both impaired fetal and placental growth, whereas deficiency in IGF-I reduces fetal growth only. Conversely, maternal IGF supplementation in early pregnancy in the guinea pig increases placental and fetal size by mid pregnancy. This study aimed to determine whether these anabolic effects persist into late pregnancy after cessation of treatment. On Day 20 of pregnancy, mothers were anaesthetised and a mini osmotic pump was implanted subcutaneously, to deliver 1mg/kg/day IGF-I (n = 7), IGF-II (n = 9) or vehicle (n = 7) for 17 days. Guinea pigs were killed on Day 62 of pregnancy (term ~67 days). Fetal and placental weights, and maternal and fetal body composition, were measured. Total litter size was unaffected by IGF treatment; however, IGF-II increased the number of viable fetuses by 26% (P = 0.01). After adjusting for the number of viable pups per litter, maternal IGF treatment increased fetal growth by increasing abdominal circumference, crown-rump length and fetal weight (fetal weight: IGF-I 79+/–2.5 g; IGF-II 78+/–2.6 g; vs vehicle 68+/–2.5 g, P = 0.02). IGF treatment did not alter absolute or relative fetal organ weights. IGF-I reduced placental weight by 9% and IGF-II increased it by 9%, but not significantly. IGF-I increased the fetal weight�:�placental weight ratio (19+/–0.9 vs 15+/–0.9, respectively P = 0.043). IGF treatment did not affect maternal weight gain during pregnancy nor net carcass weight; however, IGF-I reduced maternal lung and adipose tissue weights. In conclusion, maternal IGF-II treatment during early pregnancy improved fetal growth into late gestation, possibly by modulating placental efficiency. As poor placental development is implicated in fetal growth restriction, increasing maternal IGF abundance in early to mid pregnancy may be a potential therapeutic approach to placental insufficiency.

scholarly journals Fetal growth and ratio of placental weight to birth weight.

BMJ ◽  
1992 ◽  
Vol 304 (6833) ◽  
pp. 1052-1052
Author(s):  
D. G. Altman ◽  
J. M. Bland ◽  
L. Meyer
Keyword(s):  
Birth Weight ◽  
Fetal Growth ◽  
Placental Weight

scholarly journals Effects of Plasma Choline Concentrations on Placental Development and Fetal Growth, With Potential Mechanistic Roles of Imprinted Genes

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 755-755
Author(s):  
Olivia Gutherz ◽  
Jia Chen ◽  
Qian Li ◽  
Maya Deyssenroth ◽  
Neil Dodge ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drug Use ◽  
Fetal Growth ◽  
Regression Models ◽  
Alcohol Exposure ◽  
Interaction Effects ◽  
Placental Weight ◽  
Imprinted Genes ◽  
Placental Development ◽  
Imprinted Gene

Abstract Objectives Imprinted genes are epigenetically regulated and play critical roles in placental development and fetal growth. We aimed to examine (1) the impact of maternal one-carbon (methyl donor) nutrition on placental imprinted gene expression, placental development, and fetal growth; (2) whether imprinted gene expression alterations mediate effects of one-carbon nutrition on placental development and fetal growth; (3) interaction effects between one-carbon nutrients and imprinted genes in placental development and fetal growth. Methods Histopathology and expression of 109 imprinted genes (Nanostring) were assessed in placentas from 101 women recruited at initiation of antenatal care in a prospective cohort study examining developmental effects of prenatal alcohol exposure in South Africa. Women were interviewed prenatally about demographics, alcohol, smoking, and drug use, and erythrocyte folate, serum vitamin B12, and plasma choline concentrations were assayed at recruitment. Infant weight and height were assessed at age 2 wk. Results In limma tests, women with plasma choline concentrations below the median had lower placental expression of EPS15, IGF2R, LINC00657, SGCE, ZC3H12C, and ZNF264 than women above the median (p &lt; .05, FDR &lt; .10). In regression models adjusted for potential confounders (maternal age, gravidity, education, alcohol and drug use), plasma choline (μM) was associated with larger placental weight (g) (B = 14.0(1.9, 26.2)) and reduced maternal vascular underperfusion (MVU) prevalence (B = −.07(−.12, −.02). In causal inference analyses, there were trends for mediation of the relation between choline and MVU by decreased LINC00657, ZC3H12C, and ZNF264 expression. In regression models examining plasma choline X imprinted gene expression interaction effects, choline modified relations of EPS15, ZC3H12C, and ZNF264 to placental weight and fetal growth. Conclusions Maternal plasma choline was associated with decreased placental expression of 6 imprinted genes, 3 of which may mediate effects of choline on placental development. Choline modified effects of 3 genes on placental and fetal growth. These findings suggest maternal choline status may impact placental and fetal development, with imprinted genes playing mechanistic roles. Funding Sources NIH/NIAAA; Lycaki-Young Fund.

Antenatal Vitamin D Preserves Placental Vascular and Fetal Growth in Experimental Chorioamnionitis Due to Intra-amniotic Endotoxin Exposure

2018 ◽  
Vol 35 (13) ◽  
pp. 1260-1270 ◽  
Author(s):  
Michael Cookson ◽  
Sharon Ryan ◽  
Gregory Seedorf ◽  
R. Dodson ◽  
Steve Abman ◽  
...  
Keyword(s):  
Vitamin D ◽  
Birth Weight ◽  
Fetal Growth ◽  
Vascular Development ◽  
Vessel Density ◽  
Placental Weight ◽  
Late Gestation ◽  
Saline Control ◽  
Protective Effects ◽  
High Power Field

Background Chorioamnionitis (CA) is associated with a high risk for the development of bronchopulmonary dysplasia (BPD) after preterm birth, but mechanisms that increase susceptibility for BPD and strategies to prevent BPD are uncertain. As a model of CA, antenatal intra-amniotic (IA) endotoxin (ETX) exposure alters placental structure, causes fetal growth restriction, increases perinatal mortality, and causes sustained cardiorespiratory abnormalities throughout infancy. Vitamin D (Vit D) has been shown to have both anti-inflammatory and proangiogenic properties. Antenatal IA treatment with Vit D (1,25-(OH)2D3) during IA ETX exposure improves survival and increases vascular and alveolar growth in infant rats. Whether IA ETX causes decreased placental vascular development and if the protective effects of prenatal Vit D treatment are due to direct effects on the fetus or to improved placental vascular development remain unknown. Objective The objective of this study was to determine if IA ETX impairs placental vascular development and Vit D metabolism, and whether 1,25-(OH)2D3 treatment improves placental vascularity after IA ETX exposure during late gestation in pregnant rats. Design/Methods Fetal rats were exposed to ETX (10 mg), ETX + 1,25-(OH)2D3 (1 ng/mL), 1,25-(OH)2D3 (1 ng/mL), or saline (control) via IA injection at E20 and delivered 2 days later. To assess placental vascular development, histologic sections from the placenta were stained for CD31 and vessel density per high power field (HPF) was determined and analyzed using Matlab software. To determine the effects of ETX on placental Vit D metabolism, Vit D receptor (VDR) and activity of the Vit D conversion enzyme, CYP27B1, were assayed from placental homogenates. Angiogenic mediators were measured by reverse transcription polymerase chain reaction by RNA extracted from placental tissue. Results IA ETX reduced placenta and newborn birth weights by 22 and 20%, respectively, when compared with controls (placental weight: 0.60 vs. 0.47 g; p < 0.0001; birth weight: 4.68 vs. 5.88 g; p < 0.0001). IA 1,25-(OH)2D3 treatment increased birth weight by 12% in ETX-exposed pups (5.25 vs. 4.68 g; p < 0.001). IA ETX decreased placental vessel density by 24% in comparison with controls (1,114 vs. 848 vessels per HPF; p < 0.05). Treatment with IA 1,25-(OH)2D3 increased placenta vessel density twofold after ETX exposure (1,739 vs. 848); p < 0.0001), and increased vessel density compared with saline controls by 56% (1,739 vs. 1,114; p < 0.0001). IA ETX decreased both VDR and CYP27B1 expression by 83 and 35%, respectively (p < 0.01). Conclusion IA ETX decreases placental growth and vessel density and decreases placental VDR and CYP27B1 protein expression, and that antenatal 1,25-(OH)2D3 restores placental weight and vessel density, as well as birth weight. We speculate that 1,25-(OH)2D3 treatment preserves placental function in experimental CA and that these effects may be mediated by increased vascular growth.

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