scholarly journals Effects of maternal iron restriction in the rat on hypoxia-induced gene expression and fetal metabolite levels

2001 ◽  
Vol 85 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Rohan M. Lewis ◽  
Lynwen A. James ◽  
Junlong Zhang ◽  
Christopher D. Byrne ◽  
C. Nicholas Hales
Keyword(s):  
Amino Acids ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Plasma Levels ◽  
Plasma Cholesterol ◽  
Maternal Plasma ◽  
Fetal Growth Retardation ◽  
Restricted Diet ◽  
Fetal Plasma ◽  
Restricted Group

The mechanism by which maternal Fe deficiency in the rat causes fetal growth retardation has not been clearly established. This study compared the effects on the fetuses from dams fed a control diet with two groups of dams fed Fe-restricted diets. One Fe-restricted group was fed the Fe-restricted diet for 1 week prior to mating and throughout gestation and the second Fe-restricted group was fed the Fe-restricted diet for 2 weeks prior to mating and throughout gestation. On day 21 of gestation Fe-restricted dams, and their fetuses, were anaemic. Fetal weight was reduced in both Fe-restricted groups compared with controls. Expression of hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) are induced by hypoxia. The levels of HIF-1α mRNA were highest in placenta, then in kidney, heart and liver but were not different between the groups. Levels of plasma VEGF were not different between the groups. Maternal plasma triacylglycerol was decreased in the 1-week Fe-restricted dams compared with controls. Maternal plasma cholesterol and free fatty acid levels were not different between the groups. In fetal plasma, levels of triacylglycerol and cholesterol were decreased in both Fe-restricted groups. In maternal plasma, levels of a number of amino acids were elevated in both Fe-restricted groups. In contrast, levels of a number of amino acids in fetal plasma were lower in both Fe-restricted groups. Fetal plasma lactate was increased in Fe-restricted fetuses but fetal plasma glucose and β-hydroxybutyrate were not affected. These changes in fetal metabolism may contribute to fetal growth retardation in this model. This study does not support the hypothesis that the Fe-restricted fetus is hypoxic.

Placental glucose transport in heat-induced fetal growth retardation

1992 ◽  
Vol 263 (3) ◽  
pp. R578-R585 ◽  
Author(s):  
P. J. Thureen ◽  
K. A. Trembler ◽  
G. Meschia ◽  
E. L. Makowski ◽  
R. B. Wilkening
Keyword(s):  
Glucose Transport ◽  
Fetal Growth ◽  
Plasma Glucose ◽  
Growth Retardation ◽  
Glucose Consumption ◽  
Fetal Growth Retardation ◽  
Transport Capacity ◽  
Placental Perfusion ◽  
Fetal Plasma ◽  
Glucose Levels

In six ewes heat stressed from 39 to 125 days gestation and studied in a normothermic environment at 135 days, fetal and placental masses were less than in control sheep (1,645 vs. 3,112 and 149 vs. 356 g, respectively, P less than 0.01). Umbilical glucose uptakes (Rf,UP) were measured keeping maternal arterial plasma glucose at 70 mg/dl at spontaneously occurring fetal plasma glucose values (state A) and at two additional fetal glucose levels, to determine the transplacental glucose difference (delta) vs. Rf,UP relation. At normal delta of 49.2 mg/dl, Rf,UP was less in the experimental group (3.2 vs. 5.6 mg.min-1.kg fetus-1, P less than 0.05). Differences in placental perfusion and glucose consumption could not account for this result, thus indicating a reduced placental glucose transport capacity. In state A, fetal hypoglycemia enlarged significantly (P less than 0.01) the delta to 56.7 mg/dl and increased Rf,UP approximately 50% over the Rf,UP at a normal delta. In heat-induced fetal growth retardation, fetal hypoglycemia increases the flux of maternal glucose across a placenta with reduced glucose transport capacity.

Decreased Expression of PAI-2 mRNA and Protein in Pregnancies Complicated with Intrauterine Fetal Growth Retardation

1996 ◽  
Vol 76 (05) ◽  
pp. 761-767 ◽  
Author(s):  
Salvador Grancha ◽  
Amparo Estellés ◽  
Juan Gilabert ◽  
Melitina Chirivella ◽  
Francisco España ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Plasma Levels ◽  
Cell Types ◽  
Normal Pregnancy ◽  
High Plasma ◽  
Fetal Growth Retardation

SummaryAn increase in plasma plasminogen activator inhibitors (PAIs), fundamentally PAI type 2 (PAI-2), has been described in normal pregnancy probably because the placenta is the main source of the high plasma levels of this protein. Although we have previously described plasmatic alterations of these inhibitors in pregnancies complicated with intrauterine fetal growth retardation (IUGR), no reports have been published about placental PAI-2 mRNA expression. In the present study, the placental PAI-2 expression determined in pregnancies complicated with IUGR and in severe preeclamptic patients was compared with that of normal pregnancies in order to identify the placental cell types expressing PAI-2 and to determine whether the production of PAI-2 is altered in placentas from IUGR. In situ hybridization analyses show that the syncytiotrophoblasts are the cells with the greatest PAI-2 expression in placenta. We report that the significant decrease in plasma and placental PAI-2 levels in IUGR groups is fundamentally due to a diminished expression of PAI-2 mRNA in placenta.

Fetal growth inhibition and decreased thyroid activity after injection of oestradiol benzoate into pregnant rats

1982 ◽  
Vol 93 (1) ◽  
pp. 55-63 ◽  
Author(s):  
E. R. Kühn ◽  
M. Bollen ◽  
V. Darras
Keyword(s):  
Fetal Growth ◽  
Plasma Levels ◽  
Close Correlation ◽  
Maternal Plasma ◽  
Pregnant Rats ◽  
Fetal Plasma ◽  
Glucose Levels ◽  
Oestradiol Benzoate ◽  
Placental Blood ◽  
Circulating Levels

Pregnant rats were subcutaneously injected daily with 10 μg oestradiol benzoate (OB) and/or 1 mg bromocriptine starting on day 15 of gestation. After treatment with OB, but not bromocriptine, lower fetal body weight, fetal length and placental weight were observed. The administration of bromocriptine did not influence maternal plasma levels of prolactin, but fetal levels were decreased on day 22 of gestation. Oestradiol benzoate raised prolactin concentrations in maternal plasma on days 20 and 22, whereas fetal plasma levels were raised on day 22. This increase was counteracted by simultaneous administration of bromocriptine and OB, whereas impairment of fetal growth remained after treatment. A slight decline in fetal plasma levels of insulin was observed once, but thyroid content of triiodothyronine and thyroxine (T4) was decreased to a quarter and a third respectively of control levels in male and female fetuses of OB-treated rats, fetal circulating levels of T4 were also depressed. Maternal and fetal plasma glucose levels were decreased. A close correlation between T4 and placental or fetal weight was always present on day 22 of gestation. It was concluded that OB injected into pregnant rats will reach the fetal circulation as judged by increases in fetal plasma levels of prolactin. The observed fetal growth retardation after the OB injection was associated with thyroid deficiency, whereas plasma levels of prolactin and insulin were either not at all or only slightly altered. A direct effect of OB on placental blood flow and hence on the fetal food supply cannot, however, be excluded.

A Prospective Study of Haemostatic Tests at 28 Weeks Gestation as Predictors of Pre-Eclampsia and Growth Retardation

1989 ◽  
Vol 61 (02) ◽  
pp. 243-245 ◽  
Author(s):  
J G Thornton ◽  
B J Molloy ◽  
P S Vinall ◽  
P R Philips ◽  
R Hughes ◽  
...  
Keyword(s):  
Discriminant Analysis ◽  
Prospective Study ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Degradation Products ◽  
Fetal Growth Retardation ◽  
Fibrin Degradation Products ◽  
A Prospective Study ◽  
Primiparous Women ◽  
Significant Model

SummaryA panel of haemostatic tests was perfomed on 400 primiparous women at 28 weeks to test whether one or more could predict the development of pregnancy complications. Fifteen women subsequently developed pre-eclampsia with significant proteinuria and 13 delivered growth retarded infants. There were no significant differences between mothers in the pre-eclampsia group and 22 randomly selected controls. A stepwise logistic discriminant analysis of the data did not produce a significant model. In the growth retarded group only beta thromboglobulin levels were significantly lower than in the controls (p <0.05), although in the logistic discriminant analysis the inclusion of both beta thromboglobulin and fibrin degradation products led to a borderline significant improvement in fit of the model. We conclude that the haemostatic variables studied are not significantly changed at 28 weeks nor clinically useful predictors of either pre-eclampsia or fetal growth retardation.

Uteroplacental hemodynamic disturbances in establishment of fetal growth retardation in streptozocin-induced diabetic rats

Diabetes ◽  
1990 ◽  
Vol 39 (6) ◽  
pp. 743-746 ◽  
Author(s):  
N. C. Chartrel ◽  
M. T. Clabaut ◽  
F. A. Boismare ◽  
J. C. Schrub
Keyword(s):  
Fetal Growth ◽  
Growth Retardation ◽  
Diabetic Rats ◽  
Fetal Growth Retardation

VITAMIN D DEFICIENCY AND SYNDROME FETAL GROWTH RETARDATION

2020 ◽  
Vol 22 (3) ◽  
pp. 13-17
Author(s):  
Bushueva E.V. ◽  
◽  
Levitskaya V.M. ◽  
Boboeva Sh.G. ◽  
Sidorova T.N. ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Fetal Growth Retardation
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