scholarly journals Placental corticotrophin releasing hormone is a modulator of fetal liver blood perfusion

2020 ◽  
Author(s):  
Satoru Ikenoue ◽  
Feizal Waffarn ◽  
Masanao Ohashi ◽  
Mamoru Tanaka ◽  
Daniel L Gillen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Composition ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Umbilical Vein ◽  
Liver Blood Flow ◽  
Late Gestation ◽  
Ductus Venosus ◽  
Maternal Circulation ◽  
Releasing Hormone

Abstract Context Variation in fetal liver blood flow influences fetal growth and postnatal body composition. Placental corticotrophin-releasing hormone has been implicated as a key mediator of placental-fetal perfusion. Objective To determine whether circulating levels of placental corticotrophin-releasing hormone across gestation are associated with variations in fetal liver blood flow. Design Prospective cohort study Methods Fetal ultrasonography was performed at 30 weeks’ gestation to characterize fetal liver blood flow (quantified by subtracting ductus venosus flow from umbilical vein flow). Placental corticotrophin-releasing hormone was measured in maternal circulation at approximately 12, 20 and 30 weeks’ gestation. Multiple regression analysis was used to determine the proportion of variation in fetal liver blood flow explained by placental corticotrophin-releasing hormone. Co-variates included maternal age, parity, pre-pregnancy BMI, gestational weight gain, and fetal sex. Results A total of 79 uncomplicated singleton pregnancies were analyzed. Fetal liver blood flow was 68.4 ± 36.0 ml/min (mean ± SD). Placental corticotrophin-releasing hormone concentrations at 12, 20 and 30 weeks were 12.5 ± 8.1, 35.7 ± 24.5 and 247.9 ± 167.8 pg/ml, respectively. Placental corticotrophin-releasing hormone at 30 weeks, but not at 12 and 20 weeks, was significantly and positively associated with fetal liver blood flow at 30 weeks (r = 0.319, p = 0.004), and explained 10.4% of the variance in fetal liver blood flow. Conclusions Placental corticotrophin-releasing hormone in late gestation is a possible modulator of fetal liver blood flow, and may constitute a biochemical marker in clinical investigations of fetal growth and body composition.

316. MATERNAL DIETARY ARGININE SUPPLEMENTATION DURING LATE GESTATION IMPROVES REPRODUCTIVE EFFICIENCY IN PIGS

2010 ◽  
Vol 22 (9) ◽  
pp. 116
Author(s):  
M. J. De Blasio ◽  
C. T. Roberts ◽  
K. Kind ◽  
R. Smits ◽  
M. Nottle ◽  
...  
Keyword(s):  
Blood Flow ◽  
Birth Weight ◽  
Fetal Growth ◽  
Umbilical Vein ◽  
Late Gestation ◽  
Critical Periods ◽  
Placental Development ◽  
Pregnant Rats ◽  
Growth And Survival ◽  
Arginine Supplementation

Arginine (a non-essential amino acid) and its conversion to nitric oxide (NO) can promote formation of new blood vessels and cause vasodilation. This may reduce resistance and increase blood flow to the uterus and placenta, and the delivery of nutrients for fetal growth and survival. In pregnant rats, dietary arginine deficiency causes IUGR and increases fetal death and perinatal mortality, whereas dietary arginine supplementation reverses this. Human IUGR is associated with impaired NO synthesis, and eNOS activity in umbilical vein endothelial cells, but maternal arginine supplements have produced inconclusive results. We hypothesised that maternal arginine supplementation (MAS) in the pig (a species with naturally occurring IUGR), during late gestation, when placental angiogenesis and vascularity increase, would increase birth and placental weights. Large White (LW) and Landrace (LR) gilts (n = 285) and sows (n = 326), were fed either a control or arginine supplemented (+25 g/d arginine, Nutreco Progenos premix) diet (2.5 kg/d) in late gestation (d75-term at ~114 days). Number born, born alive, still born and mummified, birth weight and d10 weight of progeny were measured. Data were analysed using Univariate ANOVA. MAS in late gestation in gilts and sows reduced the number of still born (Con: 1.17 ± 0.13 piglets/litter; Arg: 0.84 ± 0.09 piglets/litter; P = 0.046). In LW gilts, MAS increased birth weight (Con: 1.21 ± 0.05kg; Arg: 1.34 ± 0.05kg; P < 0.05), and litter birth weight (Con: 13.38 ± 0.72 kg; Arg: 15.27 ± 0.73 kg; P < 0.05). MAS also increased birth weight in LW (Con: 1.17 ± 0.06 kg; Arg: 1.30 ± 0.06 kg; P < 0.05) and LR (Con: 1.47 ± 0.05 kg; Arg: 1.60 ± 0.05 kg; P < 0.05) sows, and reduced still borns in LW sows (Con: 1.12 ± 0.14 piglets/litter; Arg: 0.77 ± 0.09 piglets/litter; P < 0.05). MAS in late gestation improves pregnancy outcomes in terms of piglet survival and birth weight, in LW and LR gilts and sows. MAS during critical periods of placental development may enhance placental-fetal blood flow and nutrient transfer, thereby improving fetal growth and survival.

Role of ductus venosus in distribution of umbilical blood flow in human fetuses during second half of pregnancy

2000 ◽  
Vol 279 (3) ◽  
pp. H1256-H1263 ◽  
Author(s):  
Maria Bellotti ◽  
Giancarlo Pennati ◽  
Camilla De Gasperi ◽  
Frederick C. Battaglia ◽  
Enrico Ferrazzi
Keyword(s):  
Blood Flow ◽  
Fetal Liver ◽  
Color Doppler ◽  
Liver Perfusion ◽  
Normal Pregnancy ◽  
Left Lobe ◽  
Ductus Venosus ◽  
Venous Circulation ◽  
Umbilical Blood ◽  
Umbilical Blood Flow

Color Doppler sonography was used to study umbilical and ductus venosus (DV) flow in 137 normal fetuses between 20 and 38 wk of gestation. Hepatic flows were also evaluated. In all parts of the venous circulation examined, blood flow increased significantly with advancing gestational age. The weight-specific amniotic umbilical flow did not change significantly during gestation (120 ± 44 ml · min−1 · kg−1), whereas DV flow decreased significantly (from 60 to 17 ml · min−1 · kg−1). The percentage of umbilical blood flow shunted through the DV decreased significantly (from 40% to 15%); consequently, the percentage of flow to the liver increased. The right lobe flow changed from 20 to 45%, whereas the left lobe flow was approximately constant (40%). These changes are related to different patterns of growth of the umbilical veins and DV diameters. The present data support the hypothesis that the DV plays a less important role in shunting well-oxygenated blood to the brain and myocardium in late normal pregnancy than in early gestation, which leads to increased fetal liver perfusion.

scholarly journals The effect of a maternal meal on fetal liver blood flow

PLoS ONE ◽  
2019 ◽  
Vol 14 (6) ◽  
pp. e0216176
Author(s):  
Gun Lisbet Opheim ◽  
Tore Henriksen ◽  
Guttorm Haugen
Keyword(s):  
Blood Flow ◽  
Fetal Liver ◽  
Liver Blood Flow

scholarly journals EP12.09: Umbilical vein blood flow at 11-13 weeks of gestation in twin pregnancy is associated with fetal growth

2018 ◽  
Vol 52 ◽  
pp. 252-252
Author(s):  
M. Goto ◽  
H. Takita ◽  
T. Arakaki ◽  
M. Tokunaka ◽  
T. Oba ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Twin Pregnancy ◽  
Umbilical Vein

Endocrine regulation of fetal growth

1995 ◽  
Vol 7 (3) ◽  
pp. 351 ◽  
Author(s):  
AL Fowden
Keyword(s):  
Gene Expression ◽  
Growth Factors ◽  
Fetal Growth ◽  
Growth Regulation ◽  
Fetal Liver ◽  
In Utero ◽  
Tissue Differentiation ◽  
Late Gestation ◽  
Endocrine Regulation ◽  
Tissue Accretion

Hormones have an important role in the control of fetal growth. They act on both tissue accretion and differentiation and enable a precise and orderly pattern of growth to occur during late gestation. In part, their actions on growth may be mediated by other growth factors such as the insulin-like growth factors (IGFs). Insulin stimulates fetal growth by increasing the mitotic drive and nutrient availability for tissue accretion. It has little effect on tissue differentiation. In contrast, the main effects of cortisol in utero are on tissue differentiation and maturation. Cortisol appears to act directly on the cells to alter gene transcription or post-translational processing of the gene products. Cortisol may also initiate the transition from the fetal to the adult modes of growth regulation by inducing the switch from IGF-II to IGF-I gene expression in the fetal liver. Thyroxine affects both tissue accretion and differentiation in the fetus by a combination of metabolic and non-metabolic mechanisms. Pituitary growth hormone, on the other hand, appears to have little part in the control of fetal growth, unlike its role postnatally. Fetal hormones, therefore, promote growth and development in utero by altering both the metabolism and gene expression of the fetal tissues. These hormonal actions ensure that fetal growth rate is commensurate with the nutrient supply and that prepartum maturation occurs in preparation for extrauterine life.

scholarly journals Loss of the pregnancy-induced rise in cortisol concentrations in the ewe impairs the fetal insulin-like growth factor axis

2011 ◽  
Vol 23 (5) ◽  
pp. 665 ◽  
Author(s):  
Ellen C. Jensen ◽  
Laura Bennet ◽  
Charles Wood ◽  
Mark Vickers ◽  
Bernhard Breier ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Plasma Concentrations ◽  
Late Gestation ◽  
Control Group ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Igf I ◽  
Low Cortisol

Maternal cortisol levels increase during pregnancy. Although this change is important for optimal fetal growth, the mechanisms of the changes in growth remain unclear. The hypothesis examined was that alterations in maternal plasma cortisol concentrations are associated with changes in the fetal insulin-like growth factor (IGF) axis. Pregnant ewes in late gestation (115 ± 0.4 days) were studied: six control animals, five ewes given 1 mg kg–1 day–1 cortisol (high cortisol) and five adrenalectomised ewes given 0.5–0.6 mg kg–1 day–1 cortisol (low cortisol). Blood samples were taken throughout the experiment and at necropsy (130 ± 0.2 days) and fetal liver was frozen for mRNA analysis. Fetal IGF-I and insulin plasma concentrations were lower and insulin-like growth factor-binding protein-1 (IGFBP-1) concentrations were higher in the low cortisol group compared with those in the control group (P < 0.05). Fetal liver IGF-II and IGFBP-3 mRNA were decreased in low cortisol animals compared with controls (P < 0.05). There were no significant changes in these parameters in the high cortisol group, and there were no changes in fetal liver IGF-I, growth hormone receptor, IGF-I receptor, IGF-II receptor, IGFBP-1 or IGFBP-2 mRNA levels between the groups. These data suggest that reduced fetal IGF availability contributes to reduced fetal growth when maternal cortisol secretion is impaired, but not during exposure to moderate increases in cortisol.

Differential regulation of suppressor of cytokine signaling-3 in the liver and adipose tissue of the sheep fetus in late gestation

2006 ◽  
Vol 290 (4) ◽  
pp. R1044-R1051 ◽  
Author(s):  
Sheridan Gentili ◽  
Michael J. Waters ◽  
I. Caroline McMillen
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Late Gestation ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Perirenal Adipose Tissue ◽  
Plasma Prl ◽  
Sheep Fetus

It is unknown whether the JAK/STAT/suppressor of cytokine signaling-3 (SOCS-3) intracellular signaling pathway plays a role in tissue growth and metabolism during fetal life. We investigated whether there is a differential profile of SOCS-3 expression in the liver and perirenal adipose tissue during the period of increased fetal growth in late gestation and the impact of fetal growth restriction on SOCS-3 expression in the fetal liver. We also determined whether basal SOCS-3 expression in the fetal liver and perirenal adipose tissue is regulated by endogenous fetal prolactin (PRL). SOCS-3 mRNA abundance was higher in the liver than in the pancreas, spleen, and kidney of the sheep fetus during late gestation. In the liver, SOCS-3 mRNA expression was increased ( P < 0.05) between 125 ( n = 4) and 145 days ( n = 7) gestation and lower ( P < 0.05) in growth-restricted compared with normally grown fetal sheep in late gestation. The relative expression of SOCS-3 mRNA in the fetal liver was directly related to the mean plasma PRL concentrations during a 48-h infusion of either a dopaminergic agonist, bromocriptine ( n = 7), or saline ( n = 5), such that SOCS-3 mRNA expression was lower when plasma PRL concentrations decreased below ∼20 ng/ml [ y = 0.99 − (2.47/ x) + (4.96/ x2); r2 = 0.91, P < 0.0001, n = 12]. No relationship was shown between the abundance of phospho-STAT5 in the fetal liver and circulating PRL. SOCS-3 expression in perirenal adipose tissue decreased ( P < 0001) between 90–91 ( n = 6) and 140–145 days ( n = 9) gestation and was not related to endogenous PRL concentrations. Thus SOCS-3 is differentially expressed and regulated in key fetal tissues and may play an important and tissue-specific role in the regulation of cellular proliferation and differentiation before birth.

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