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Colin P Sibley

defective placentation and the consequently dysfunctional placenta is a direct cause of what has been termed the ‘Great Obstetrical Syndromes’: pre-eclampsia, fetal growth restriction (FGR), preterm labour, preterm premature rupture of membranes, late

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Melissa A Davis, Leticia E Camacho, Alexander L Pendleton, Andrew T Antolic, Rosa I Luna-Ramirez, Amy C Kelly, Nathan R Steffens, Miranda J Anderson, and Sean W Limesand

2009 The transition from fetal growth restriction to accelerated postnatal growth: a potential role for insulin signalling in skeletal muscle . Journal of Physiology 587 4199 – 4211 . ( https://doi.org/10.1113/jphysiol.2009.173161 ) Murotsuki

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Karen Forbes and Melissa Westwood

Introduction Aberrant fetal growth affects as many as 7% of babies – ∼50 000 infants born each year in the UK ( Population, Censuses & Surveys Office 2007 ). Many infants born with inadequate growth (fetal growth restriction; FGR) die, and others

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Jacqueline M Wallace

proposed as a primary driver of the placental dysfunction underlying preeclampsia, fetal growth restriction and preterm delivery in young human adolescents ( Brosens et al. 2017 ) and the suggestion that preconditioning of the immature uterus by exposure

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Thorsten Braun, Shaofu Li, Timothy J M Moss, John P Newnham, John R G Challis, Peter D Gluckman, and Deborah M Sloboda

-induced fetal growth restriction. Therefore, we investigated the effects of maternal betamethasone (BET) administration on the numbers and distribution of placental BNCs, on placental oPL protein levels, and on maternal and fetal plasma oPL levels in sheep

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J Lesage, D Hahn, M Leonhardt, B Blondeau, B Breant, and JP Dupouy

Fetal intrauterine growth restriction (IUGR) is a frequently occurring and serious complication of pregnancy. Infants exposed to IUGR are at risk for numerous perinatal morbidities, including hypoglycemia in the neonatal period, as well as increased risk of later physical and/or mental impairments, cardiovascular disease and non-insulin-dependent diabetes mellitus. Fetal growth restriction most often results from uteroplacental dysfunction during the later stage of pregnancy. As glucose, which is the most abundant nutrient crossing the placenta, fulfills a large portion of the fetal energy requirements during gestational development, and since impaired placental glucose transport is thought to result in growth restriction, we investigated the effects of maternal 50% food restriction (FR50) during the last week of gestation on rat placental expression of glucose transporters, GLUT1, GLUT3 and GLUT4, and on plasma glucose content in both maternal and fetal compartments. Moreover, as maternal FR50 induces fetal overexposure to glucocorticoids and since these hormones are potent regulators of placental glucose transporter expression, we investigated whether putative alterations in placental GLUT expression correlate with changes in maternal and/or fetal corticosterone levels. At term (day 21 of pregnancy), plasma glucose content was significantly reduced (P<0.05) in mothers subjected to FR50, but was not affected in fetuses. Food restriction reduced maternal body weight (P<0.001) but did not affect placental weight. Plasma corticosterone concentration, at term, was increased (P<0.05) in FR50 mothers. Fetuses from FR50 mothers showed reduced body weight (P<0.001) but higher plasma corticosterone levels (P<0.05). Adrenalectomy (ADX) followed by corticosterone supplementation of the mother prevented the FR50-induced rise in maternal plasma corticosterone at term. Food restriction performed on either sham-ADX or ADX mothers induced a similar reduction in the body weight of the pups at term (P<0.01). Moreover, plasma corticosterone levels were increased in pups from sham-ADX FR50 mothers (P<0.01) and in pups from ADX control mothers (P<0.01). Western blot analysis of placental GLUT proteins showed that maternal FR50 decreased placental GLUT3 protein levels in all experimental groups at term (P<0.05 and P<0.01), but did not affect either GLUT1 or GLUT4 protein levels. Northern blot analysis of placental GLUT expression showed that both GLUT1 and GLUT3 mRNA were not affected by the maternal feeding regimen or surgery. We concluded that prolonged maternal malnutrition during late gestation decreases maternal plasma glucose content and placental GLUT3 glucose transporter expression, but does not obviously affect fetal plasma glucose concentration. Moreover, the present results are not compatible with a role of maternal corticosterone in the development of growth-restricted rat fetuses.

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K M Jeckel, A C Boyarko, G J Bouma, Q A Winger, and R V Anthony

stage for fetal growth restriction during late gestation. Materials and methods All procedures conducted with animals and lentivirus were approved by the Colorado State University Institutional Animal Care and Use Committee (Protocol 14-5257A

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Anthony M Belenchia, Sarah A Johnson, Mark R Ellersieck, Cheryl S Rosenfeld, and Catherine A Peterson

VDD and fetal growth restriction ( Miliku et al . 2016 ); however, this effect appears to be highly dependent on the severity of hypovitaminosis D and when during pregnancy the deficiency is experienced ( Leffelaar et al . 2010 , Burris et al

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Laura D Brown

hypertrophy as evidenced by fewer myofibers but larger fiber cross-sectional area compared with controls ( Fahey et al . 2005 b , Zhu et al . 2006 ). The phenomenon of postnatal catch-up growth after fetal growth restriction has been well described in a

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Casey D Wright, Ryan J Orbus, Timothy R H Regnault, and Russell V Anthony

increase in uteroplacental weight ( Wallace et al . 2004 ) was only seen in adolescent ewes maintained on a high dietary intake, a feeding regimen used in adolescent ewes to generate fetal growth restriction ( Wallace et al . 1997 , Anthony et al . 2003