scholarly journals In utero substrate restriction by placental insufficiency or maternal undernutrition decreases optical redox ratio in fetal perirenal fat

2021 ◽  
Author(s):  
Joanna Lazniewska ◽  
Jack R. T. Darby ◽  
Stacey L. Holman ◽  
Alexandra Sorvina ◽  
Sally E. Plush ◽  
...  
Keyword(s):  
In Utero ◽  
Placental Insufficiency ◽  
Redox Ratio ◽  
Maternal Undernutrition ◽  
Perirenal Fat

scholarly journals Low dose unfractionated heparin with low dose aspirin in treatment of thrombo prophylaxis in utero placental insufficiency: a new vision in heparinization during pregnancy

2018 ◽  
Vol 7 (12) ◽  
pp. 4849
Author(s):  
M. Madhubala ◽  
C. Kasthuri ◽  
Mansi Shukul ◽  
J. Mohamed Ali
Keyword(s):  
Unfractionated Heparin ◽  
Live Birth ◽  
Low Dose ◽  
Gestational Hypertension ◽  
In Utero ◽  
Placental Insufficiency ◽  
Optimal Dosage ◽  
Intrauterine Death ◽  
Dose Aspirin ◽  
Low Dose Aspirin

Background: The use of heparin and aspirin in obstetric care has grown considerably since their introduction into clinical practice. Because of the physiological changes of pregnancy, the usage of heparin and optimal dosage of heparin remains uncertain. Here our institute designed low dose Unfractionated Heparin (5000 IU s/c daily) as thrombo Prophylaxis regimen. To study the outcome of low dose UFH (5000 IU sc /daily) + Low dose aspirin (75 mg oral per day) for thrombo prophylaxis in utero placental insufficiency, in patient with 2 or more abortions.Methods: This retrospective study was conducted in 135 patients with 2 or more abortions as obstetric history. Prophylactic low dose of UFH (5000 IU s/c daily) + LDA 75 mg oral was initiated.  The Primary outcome is live birth, and secondary outcomes is Reduced incidence of early onset of gestational hypertension (HT), Intrauterine Growth Retardation (IUGR).Results: Out of 135 women 131 gave live birth, 2 had first trimester abortion and 2 had intrauterine death by 5 to 6 months. PIH was higher in patients with more than 30 years of age.Conclusions: In our Retrospective, data combination of low dose UFH (5000IU s/c) + LDA (75mg oral) is as safe as routine thrombo prophylaxis with good compliance.

scholarly journals Maternal low protein diet programmes low ovarian reserve in offspring

Reproduction ◽  
2018 ◽  
Author(s):  
Amy L Winship ◽  
Sarah E Gazzard ◽  
Luise A Cullen McEwen ◽  
John F Bertram ◽  
Karla J Hutt
Keyword(s):  
Ovarian Reserve ◽  
Histological Analysis ◽  
Maternal Diet ◽  
Primordial Follicle ◽  
In Utero ◽  
Primordial Follicles ◽  
Maternal Undernutrition ◽  
Low Protein ◽  
Pregnancy And Lactation ◽  
In Utero Development

The ovarian reserve of primordial follicle oocytes is formed during in utero development and represents the entire supply of oocytes available to sustain female fertility. Maternal undernutrition during pregnancy and lactation diminishes offspring ovarian reserve in rats. In mice, maternal oocyte maturation is also susceptible to undernutrition, causing impaired offspring cardiovascular function. We aimed to determine whether programming of the ovarian reserve is impacted in offspring when maternal undernutrition extends from preconception oocyte development through to weaning. C57BL6/J female mice were fed normal protein (20%) or low protein (8%) diet during preconception, pregnancy and lactation periods. Maternal ovaries were harvested at weaning and offspring ovaries collected at postnatal day (PN)21 and 24 weeks of age. Total follicle estimates were obtained by histologically sampling one ovary per animal (n=5/group). There was no impact of diet on maternal follicle numbers. However, in offspring, maternal protein restriction significantly depleted primordial follicles by 37% at PN21 and 51% at 24 weeks (p<0.05). There were no effects of diet on other follicle classes. Histological analysis showed no differences in the proportion of proliferative follicles (pH3-positive), but increased atresia (cleaved caspase-3-positive, or TUNEL-positive) was detected in ovaries of protein-restricted offspring at both ages (p<0.05). Our data show that maternal diet during the preconception period, in utero development and early life has significant impacts on follicle endowment and markers of follicle health later in life. This highlights the need for further investigation into the importance of maternal preconception diet for offspring reproductive development and health.

scholarly journals High Prevalence of Hypertension and Placental Insufficiency, but No In Utero HIV Transmission, among Women on HAART with Stillbirths in Botswana

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e31580 ◽  
Author(s):  
Roger L. Shapiro ◽  
Sajini Souda ◽  
Natasha Parekh ◽  
Kelebogile Binda ◽  
Mukendi Kayembe ◽  
...  
Keyword(s):  
Hiv Transmission ◽  
In Utero ◽  
Placental Insufficiency ◽  
High Prevalence

scholarly journals Fetal undernutrition, placental insufficiency, and pancreatic β-cell development programming in utero

2018 ◽  
Vol 315 (5) ◽  
pp. R867-R878 ◽  
Author(s):  
Ramkumar Mohan ◽  
Daniel Baumann ◽  
Emilyn Uy Alejandro
Keyword(s):  
Cell Mass ◽  
The United States ◽  
In Utero ◽  
Cell Development ◽  
Placental Insufficiency ◽  
Health Concern ◽  
Potential Contribution ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Peripheral Tissues

The prevalence of obesity and type 2 (T2D) diabetes is a major health concern in the United States and around the world. T2D is a complex disease characterized by pancreatic β-cell failure in association with obesity and insulin resistance in peripheral tissues. Although several genes associated with T2D have been identified, it is speculated that genetic variants account for only <10% of the risk for this disease. A strong body of data from both human epidemiological and animal studies shows that fetal nutrient factors in utero confer significant susceptibility to T2D. Numerous studies done in animals have shown that suboptimal maternal environment or placental insufficiency causes intrauterine growth restriction (IUGR) in the fetus, a critical factor known to predispose offspring to obesity and T2D, in part by causing permanent consequences in total functional β-cell mass. This review will focus on the potential contribution of the placenta in fetal programming of obesity and TD and its likely impact on pancreatic β-cell development and growth.

scholarly journals Chorioamnionitis in Rats Precipitates Extended Postnatal Inflammatory Lymphocyte Hyperreactivity

2018 ◽  
Vol 40 (5-6) ◽  
pp. 523-533 ◽  
Author(s):  
Tracylyn R. Yellowhair ◽  
Shahani Noor ◽  
Brittney Mares ◽  
Clement Jose ◽  
Jessie C. Newville ◽  
...  
Keyword(s):  
Immune Responses ◽  
Mononuclear Cells ◽  
Fetal Brain ◽  
In Utero ◽  
Placental Insufficiency ◽  
Neurological Injury ◽  
Perinatal Brain Injury ◽  
Inflammatory Signaling ◽  
Extremely Preterm ◽  
Extremely Preterm Infants

Preterm birth is an important cause of perinatal brain injury (PBI). Neurological injury in extremely preterm infants often begins in utero with chorioamnionitis (CHORIO) or inflammation/infection of the placenta and concomitant placental insufficiency. Studies in humans have shown dysregulated inflammatory signaling throughout the placental-fetal brain axis and altered peripheral immune responses in children born preterm with cerebral palsy (CP). We hypothesized that peripheral immune responses would be altered in our well-established rat model of CP. Specifically, we proposed that isolated peripheral blood mononuclear cells (PBMCs) would be hyperresponsive to a second hit of inflammation throughout an extended postnatal time course. Pregnant Sprague-Dawley dams underwent a laparotomy on embryonic day 18 (E18) with occlusion of the uterine arteries (for 60 min) followed by intra-amniotic injection of lipopolysaccharide (LPS, 4 μg/sac) to induce injury in utero. Shams underwent laparotomy only, with equivalent duration of anesthesia. Laparotomies were then closed, and the rat pups were born at E22. PBMCs were isolated from pups on postnatal day 7 (P7) and P21, and subsequently stimulated in vitro with LPS for 3 or 24 h. A secreted inflammatory profile analysis of conditioned media was performed using multiplex electrochemiluminescent immunoassays, and the composition of inflammatory cells was assayed with flow cytometry (FC). Results indicate that CHORIO PBMCs challenged with LPS are hyperreactive and secrete significantly more tumor necrosis factor α (TNFα) and C-X-C chemokine ligand 1 at P7. FC confirmed increased intracellular TNFα in CHORIO pups at P7 following LPS stimulation, in addition to increased numbers of CD11b/c immunopositive myeloid cells. Notably, TNFα secretion was sustained until P21, with increased interleukin 6, concomitant with increased expression of integrin β1, suggesting both sustained peripheral immune hyperreactivity and a heightened activation state. Taken together, these data indicate that in utero injury primes the immune system and augments enhanced inflammatory signaling. The insidious effects of primed peripheral immune cells may compound PBI secondary to CHORIO and/or placental insufficiency, and thereby render the brain susceptible to future chronic neurological disease. Further understanding of inflammatory mechanisms in PBI may yield clinically important biomarkers and facilitate individualized repair strategies and treatments.

scholarly journals Increased fetal insulin concentrations for one week fail to improve insulin secretion or β-cell mass in fetal sheep with chronically reduced glucose supply

2013 ◽  
Vol 304 (1) ◽  
pp. R50-R58 ◽  
Author(s):  
Jinny R. Lavezzi ◽  
Stephanie R. Thorn ◽  
Meghan C. O'Meara ◽  
Dan LoTurco ◽  
Laura D. Brown ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Infusion ◽  
Cell Mass ◽  
Placental Insufficiency ◽  
Late Gestation ◽  
Β Cell ◽  
Fetal Sheep ◽  
Maternal Undernutrition ◽  
Pregnant Sheep ◽  
Glucose Supply

Maternal undernutrition during pregnancy and placental insufficiency are characterized by impaired development of fetal pancreatic β-cells. Prolonged reduced glucose supply to the fetus is a feature of both. It is unknown if reduced glucose supply, independent of other complications of maternal undernutrition and placental insufficiency, would cause similar β-cell defects. Therefore, we measured fetal insulin secretion and β-cell mass following prolonged reduced fetal glucose supply in sheep. We also tested whether restoring physiological insulin concentrations would correct any β-cell defects. Pregnant sheep received either a direct saline infusion (CON = control, n = 5) or an insulin infusion (HG = hypoglycemic, n = 5) for 8 wk in late gestation (75 to 134 days) to decrease maternal glucose concentrations and reduce fetal glucose supply. A separate group of HG fetuses also received a direct fetal insulin infusion for the final week of the study with a dextrose infusion to prevent a further fall in glucose concentration [hypoglycemic + insulin (HG+I), n = 4]. Maximum glucose-stimulated insulin concentrations were 45% lower in HG fetuses compared with CON fetuses. β-Cell, pancreatic, and fetal mass were 50%, 37%, and 40% lower in HG compared with CON fetuses, respectively ( P < 0.05). Insulin secretion and β-cell mass did not improve in the HG+I fetuses. These results indicate that chronically reduced fetal glucose supply is sufficient to reduce pancreatic insulin secretion in response to glucose, primarily due to reduced pancreatic and β-cell mass, and is not correctable with insulin.

Postnatal oxytocin alleviates adverse effects in adult rat offspring caused by maternal malnutrition

2003 ◽  
Vol 284 (3) ◽  
pp. E475-E480 ◽  
Author(s):  
Hanna Olausson ◽  
Kerstin Uvnäs-Moberg ◽  
Annica Sohlström
Keyword(s):  
Blood Pressure ◽  
Adverse Effects ◽  
Plasma Levels ◽  
Food Restriction ◽  
Plasma Corticosterone ◽  
In Utero ◽  
Adult Rats ◽  
Adult Rat ◽  
Maternal Undernutrition ◽  
Ad Libitum

Repeated oxytocin administration to adult rats causes a long-term decrease of plasma levels of corticosterone and blood pressure and stimulates growth and fat retention. Maternal undernutrition increases blood pressure and plasma corticosterone in adult offspring. We hypothesized that oxytocin treatment early in life would alleviate adverse effects of intrauterine food restriction. Male pups from ad libitum-fed and food-restricted (fed 60% of ad libitum intake) dams were injected with oxytocin or saline in days 1–14 after birth. At 4 mo, blood pressure, plasma levels of corticosterone, and adiposity were assessed. Oxytocin treatment decreased blood pressure independently of nutrition, whereas the increased plasma levels of corticosterone were lowered to normal levels in food-restricted offspring. Blood pressure and adiposity were not affected by in utero food restriction, whereas birth and adult weight were. In conclusion, postnatal events may alleviate adverse effects caused by in utero food restriction. In contrast to more severe food restriction, a moderate general food restriction during gestation had no effect on blood pressure in the offspring.

The fetal somatotropic axis during long term maternal undernutrition in sheep: evidence for nutritional regulation in utero.

Endocrinology ◽  
1995 ◽  
Vol 136 (3) ◽  
pp. 1250-1257 ◽  
Author(s):  
M K Bauer ◽  
B H Breier ◽  
J E Harding ◽  
J D Veldhuis ◽  
P D Gluckman
Keyword(s):  
In Utero ◽  
Nutritional Regulation ◽  
Somatotropic Axis ◽  
Maternal Undernutrition

Alterations in Ultrastructure of Skeletal Muscle From Newborn Guinea Pigs Following in Utero Exposure to Ethanol

1985 ◽  
Vol 43 ◽  
pp. 686-687
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie ◽  
T.B. Cole
Keyword(s):  
Skeletal Muscle ◽  
Guinea Pigs ◽  
Muscle Development ◽  
In Utero ◽  
Ethanol Exposure ◽  
Prenatally Exposed ◽  
Chronic Alcoholic ◽  
Test Kit ◽  
Food And Water Intake ◽  
Post Intubation

Ultrastructural alterations of skeletal muscle have been observed in adult chronic alcoholic patients. However, no such study has been performed on individuals prenatally exposed to ethanol. In order to determine if ethanol exposure in utero in the latter stages of muscle development was deleterious, skeletal muscle was obtained from newborn guinea pigs treated in the following manner. Six Hartly strain pregnant guinea pigs were randomly assigned to either the ethanol or the pair-intubated groups. Twice daily the 3 ethanol-treated animals were intubated with Ensure (Ross Laboratories) liquid diet containing 30% ethanol (6g/Kg pre-pregnant body weight per day) from day 35 of gestation until parturition at day 70±1 day. Serum ethanol levels were determined at 1 hour post-intubation by the Sigma alcohol test kit. For pair-intubation the Ensure diet contained sucrose substituted isocalorically for ethanol. Both food and water intake were monitored.

509: In Utero Exposure to the UV Stabilizer Benzophenone-2 Causes Hypospadias in Mice

2006 ◽  
Vol 175 (4S) ◽  
pp. 165-165
Author(s):  
Michael H. Hsieh ◽  
Erin Cheasty ◽  
Emily J. Willingham ◽  
Benchun Liu ◽  
Laurence S. Baskin
Keyword(s):  
In Utero ◽  
In Utero Exposure
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