scholarly journals Dexamethasone treatment of pregnant F0 mice leads to parent of origin-specific changes in placental function of the F2 generation

2015 ◽  
Vol 27 (4) ◽  
pp. 704 ◽  
Author(s):  
O. R. Vaughan ◽  
H. M. Phillips ◽  
A. J. Everden ◽  
A. N. Sferruzzi-Perri ◽  
A. L. Fowden
Keyword(s):  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Amino Acid Analogue ◽  
Prenatally Exposed ◽  
Dexamethasone Treatment ◽  
Placental Function ◽  
Paternal Line ◽  
Acid Analogue ◽  
Parent Of Origin ◽  
F2 Generation

Dexamethasone treatment of F0 pregnant rodents alters F1 placental function and adult cardiometabolic phenotype. The adult phenotype is transmitted to the F2 generation without further intervention, but whether F2 placental function is altered by F0 dexamethasone treatment remains unknown. In the present study, F0 mice were untreated or received dexamethasone (0.2 µg g–1 day–1, s.c.) over Days 11–15 or 14–18 of pregnancy (term Day 21). Depending on the period of F0 dexamethasone treatment, F1 offspring were lighter at birth or grew more slowly until weaning (P < 0.05). Glucose tolerance (1 g kg–1, i.p.) of adult F1 males was abnormal. Mating F1 males exposed prenatally to dexamethasone with untreated females had no effect on F2 placental function on Day 19 of pregnancy. In contrast, when F1 females were mated with untreated males, F2 placental clearance of the amino acid analogue 14C-methylaminoisobutyric acid was increased by 75% on Day 19 specifically in dams prenatally exposed to dexamethasone on Days 14–18 (P < 0.05). Maternal plasma corticosterone was also increased, but F2 placental Slc38a4 expression was decreased in these dams (P < 0.05). F0 dexamethasone treatment had no effect on F2 fetal or placental weights, regardless of lineage. Therefore, the effects of F0 dexamethasone exposure are transmitted intergenerationally to the F2 placenta via the maternal, but not paternal, line.

scholarly journals Maternal undernutrition during late gestation-induced intrauterine growth restriction in the rat is associated with impaired placental GLUT3 expression, but does not correlate with endogenous corticosterone levels

2002 ◽  
Vol 174 (1) ◽  
pp. 37-43 ◽  
Author(s):  
J Lesage ◽  
D Hahn ◽  
M Leonhardt ◽  
B Blondeau ◽  
B Breant ◽  
...  
Keyword(s):  
Body Weight ◽  
Plasma Glucose ◽  
Food Restriction ◽  
Glucose Transporter ◽  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Growth Restriction ◽  
Late Gestation ◽  
Glucose Content ◽  
Protein Levels

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.

scholarly journals Isolation and characterization of a new class of amino-acid-analogue-resistant mutants inAspergillus nidulansusing reduced carbon flow

1979 ◽  
Vol 34 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Mahavir Singh ◽  
Umakant Sinha
Keyword(s):  
Amino Acid ◽  
Aromatic Amino Acids ◽  
Sole Source ◽  
Amino Acid Analogue ◽  
Linkage Groups ◽  
Isolation And Characterization ◽  
Acid Analogue ◽  
Amino Acid Analogues ◽  
Resistant Mutants ◽  
Growth Requirement

SUMMARYFour recessive amino-acid-analogue-resistant mutants were isolated on a medium containing acetate as the sole carbon source and the amino acid analogues p-fluorophenylalanine and ethionine. None of the mutants showed any growth requirement. Analysis of growth on media containing an amino acid as the sole nitrogen source indicated that two mutants out of the four possess normal systems for utilization of acidic, neutral, basic and aromatic amino acids. The mutantsfpa70 andfpa71 showed reduced growth on tryptophan as the sole source of nitrogen. Three new loci, identified after preliminary genetic analysis, were located on three linkage groups: one each on linkage groups I, VI and VIII.

scholarly journals Growth induced translocation effectively directs an amino acid analogue to developing zones in Agaricus bisporus

2020 ◽  
Vol 124 (12) ◽  
pp. 1013-1023 ◽  
Author(s):  
Koen C. Herman ◽  
Han A.B. Wösten ◽  
Mark D. Fricker ◽  
Robert-Jan Bleichrodt
Keyword(s):  
Amino Acid ◽  
Agaricus Bisporus ◽  
Amino Acid Analogue ◽  
Acid Analogue

Influence of protein deficiency in rats on hormonal status and cytoplasmic glucocorticoid receptors in maternal and fetal tissues

1982 ◽  
Vol 95 (1) ◽  
pp. 49-58 ◽  
Author(s):  
S. Mulay ◽  
D. R. Varma ◽  
S. Solomon
Keyword(s):  
Glucocorticoid Receptors ◽  
Fetal Liver ◽  
Fetal Lung ◽  
Maternal Plasma ◽  
Plasma Corticosterone ◽  
Protein Deficiency ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Maternal Malnutrition ◽  
Sprague Dawley Rats

The influence of dietary protein deficiency on maternal plasma corticosterone and progesterone levels as well as on maternal and fetal liver and lung cytoplasmic glucocorti-coid receptors has been studied in Sprague–Dawley rats during the last 3 days of gestation. Plasma corticosterone levels of control but not protein-deficient rats increased on days 20 and 21 of gestation; corticosterone levels of protein-deficient rats decreased on day 21 of gestation. Maternal adrenalectomy caused only a moderate decrease in corticosterone levels in both groups of pregnant rats. Fetal corticosterone levels of the two groups of rats were similar. Progesterone levels were consistently lower in protein-deficient than in control animals from day 20 of gestation until 2–12 h after parturition. There were no differences in the binding of [3H]dexamethasone to liver cytosol of non-pregnant control and protein-deficient rats. However, receptor levels were lower in pregnant controls than in pregnant protein-deficient rats. Maternal protein deficiency led to an increase in fetal liver glucocorticoid receptor levels but exerted no significant effect on receptor levels in fetal lung. It is suggested that lower levels of plasma corticosterone and progesterone and high levels of liver glucocorticoid receptors in protein-deficient rats might be related to some of the adverse consequences of maternal malnutrition on fetal development.

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