Periconceptional alcohol consumption causes fetal growth restriction and increases glycogen accumulation in the late gestation rat placenta

Placenta ◽  
2014 ◽  
Vol 35 (1) ◽  
pp. 50-57 ◽  
Author(s):  
E.M. Gårdebjer ◽  
J.S.M. Cuffe ◽  
M. Pantaleon ◽  
M.E. Wlodek ◽  
K.M. Moritz
Keyword(s):  
Alcohol Consumption ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Late Gestation ◽  
Glycogen Accumulation

Prenatal alcohol consumption and fetal growth restriction: Potentiation effect by concomitant smoking

2009 ◽  
Vol 11 (1) ◽  
pp. 36-43 ◽  
Author(s):  
Muktar H. Aliyu ◽  
Ronee E. Wilson ◽  
Roger Zoorob ◽  
Kristal Brown ◽  
Amina P. Alio ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Growth Restriction ◽  
Potentiation Effect ◽  
Prenatal Alcohol

scholarly journals The impact of a human IGF-II analog ([Leu27]IGF-II) on fetal growth in a mouse model of fetal growth restriction

2016 ◽  
Vol 310 (1) ◽  
pp. E24-E31 ◽  
Author(s):  
Jayne C. Charnock ◽  
Mark R. Dilworth ◽  
John D. Aplin ◽  
Colin P. Sibley ◽  
Melissa Westwood ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Mixed Model ◽  
Maternal Serum ◽  
Growth Restriction ◽  
Placental Weight ◽  
Late Gestation ◽  
Fetal Weight ◽  
Mixed Model Analysis ◽  
The Impact

Enhancing placental insulin-like growth factor (IGF) availability appears to be an attractive strategy for improving outcomes in fetal growth restriction (FGR). Our approach was the novel use of [Leu27]IGF-II, a human IGF-II analog that binds the IGF-II clearance receptor IGF-IIR in fetal growth-restricted (FGR) mice. We hypothesized that the impact of [Leu27]IGF-II infusion in C57BL/6J (wild-type) and endothelial nitric oxide synthase knockout (eNOS−/−; FGR) mice would be to enhance fetal growth and investigated this from mid- to late gestation; 1 mg·kg−1·day−1 [Leu27]IGF-II was delivered via a subcutaneous miniosmotic pump from E12.5 to E18.5. Fetal and placental weights recorded at E18.5 were used to generate frequency distribution curves; fetuses <5th centile were deemed growth restricted. Placentas were harvested for immunohistochemical analysis of the IGF system, and maternal serum was collected for measurement of exogenously administered IGF-II. In WT pregnancies, [Leu27]IGF-II treatment halved the number of FGR fetuses, reduced fetal( P = 0.028) and placental weight variations ( P = 0.0032), and increased the numbers of pups close to the mean fetal weight (131 vs. 112 pups within 1 SD). Mixed-model analysis confirmed litter size to be negatively correlated with fetal and placental weight and showed that [Leu27]IGF-II preferentially improved fetal weight in the largest litters, as defined by number. Unidirectional 14CMeAIB transfer per gram placenta (System A amino acid transporter activity) was inversely correlated with fetal weight in [Leu27]IGF-II-treated WT animals ( P < 0.01). In eNOS−/− mice, [Leu27]IGF-II reduced the number of FGR fetuses(1 vs. 5 in the untreated group). The observed reduction in FGR pup numbers in both C57 and eNOS−/− litters suggests the use of this analog as a means of standardizing and rescuing fetal growth, preferentially in the smallest offspring.

scholarly journals Increased uterine artery blood flow in hypoxic murine pregnancy is not sufficient to prevent fetal growth restriction†

2019 ◽  
Vol 102 (3) ◽  
pp. 660-670 ◽  
Author(s):  
Sydney L Lane ◽  
Alexandrea S Doyle ◽  
Elise S Bales ◽  
Ramón A Lorca ◽  
Colleen G Julian ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Murine Model ◽  
Pregnancy Complications ◽  
Fetal Growth Restriction ◽  
Uterine Artery ◽  
Growth Restriction ◽  
Late Gestation ◽  
Artery Blood Flow ◽  
Uterine Arteries

Abstract Incomplete maternal vascular responses to pregnancy contribute to pregnancy complications including intrauterine growth restriction (IUGR) and preeclampsia. We aimed to characterize maternal vascular dysfunction in a murine model of fetal growth restriction as an approach toward identifying targetable pathways for improving pregnancy outcomes. We utilized a murine model of late-gestation hypoxia-induced IUGR that reduced E18.5 fetal weight by 34%. Contrary to our hypothesis, uterine artery blood flow as measured in vivo by Doppler ultrasound was increased in mice housed under hypobaric hypoxia (385 mmHg; 5500 m) vs normoxia (760 mmHg; 0 m). Using wire myography, uterine arteries isolated from hypoxic mice had similar vasodilator responses to the two activators A769662 and acetylcholine as those from normoxic mice, although the contribution of an increase in nitric oxide production to uterine artery vasodilation was reduced in the hypoxic vs normoxic groups. Vasoconstrictor responses to phenylephrine and potassium chloride were unaltered by hypoxia. The levels of activated adenosine monophosphate-activated protein kinase (AMPK) were reduced with hypoxia in both the uterine artery and placenta as measured by western blot and immunohistochemistry. We concluded that the rise in uterine artery blood flow may be compensatory to hypoxia but was not sufficient to prevent fetal growth restriction. Although AMPK signaling was reduced by hypoxia, AMPK was still receptive to pharmacologic activation in the uterine arteries in which it was a potent vasodilator. Thus, AMPK activation may represent a new therapy for pregnancy complications involving reduced uteroplacental perfusion.

Glucose transporter isoform-3 mutations cause early pregnancy loss and fetal growth restriction

2007 ◽  
Vol 292 (5) ◽  
pp. E1241-E1255 ◽  
Author(s):  
Amit Ganguly ◽  
Robert A. McKnight ◽  
Santanu Raychaudhuri ◽  
Bo-Chul Shin ◽  
Zhigui Ma ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Fetal Growth ◽  
Early Pregnancy ◽  
Fetal Growth Restriction ◽  
Pregnancy Loss ◽  
Glucose Transporter ◽  
Growth Restriction ◽  
Late Gestation ◽  
Null Mouse ◽  
Early Pregnancy Loss

Glucose transporter isoform-3 (GLUT3) is the trophoblastic facilitative glucose transporter. To investigate the role of this isoform in embryonic development, we created a novel GLUT3-null mouse and observed arrested early embryonic development and loss at neurulation stage when both alleles were mutated. This loss occurred despite the presence of other related isoforms, particularly GLUT1. In contrast, when a single allele was mutated, despite increased embryonic cell apoptosis, adaptive changes in the subcellular localization of GLUT3 and GLUT1 in the preimplantation embryo led to postimplantation survival. This survival was compromised by decreased GLUT3-mediated transplacental glucose transport, causing late-gestation fetal growth restriction. This yielded young male and female adults demonstrating catch-up growth, with normal basal glucose, insulin, insulin-like growth factor-I and IGF-binding protein-3 concentrations, fat and lean mass, and glucose and insulin tolerance. We conclude that GLUT3 mutations cause a gene dose-dependent early pregnancy loss or late-gestation fetal growth restriction despite the presence of embryonic and placental GLUT1 and a compensatory increase in system A amino acid placental transport. This critical life-sustaining functional role for GLUT3 in embryonic development provides the basis for investigating the existence of human GLUT3 mutations with similar consequences during early pregnancy.

FETAL GROWTH RESTRICTION WITH EARLY AND LATE MANIFESTATION, PROGNOSTIC MARKERS

2020 ◽  
pp. 27-30
Author(s):  
Yakubova D.I.
Keyword(s):  
Risk Factors ◽  
Pregnant Women ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Prenatal Screening ◽  
Prognostic Markers ◽  
Growth Restriction ◽  
Late Manifestation ◽  
Late Form ◽  
Early Manifestation

Objective of the study: Comprehensive assessment of risk factors, the implementation of which leads to FGR with early and late manifestation. To evaluate the results of the first prenatal screening: PAPP-A, B-hCG, made at 11-13 weeks. Materials and Methods: A retrospective study included 110 pregnant women. There were 48 pregnant women with early manifestation of fetal growth restriction, 62 pregnant women with late manifestation among them. Results of the study: The risk factors for the formation of the FGR are established. Statistically significant differences in the indicators between groups were not established in the analyses of structures of extragenital pathology. According to I prenatal screening, there were no statistical differences in levels (PAPP-A, b-hCG) in the early and late form of FGR.

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