Dataset Information

Ovine fetal renal development impacted by multiple fetuses and uterine space restriction.

ABSTRACT: Intrauterine growth restriction (IUGR) from uteroplacental dysfunction causes impaired nephrogenesis and ultimately hypertension, but it is unknown whether IUGR caused by insufficient space for placental development seen in uterine anomalies and/or multifetal gestation exerts the same effects. Fetal renal development and metabolism were studied in an ovine space-restriction model by combining unilateral horn surgical ligation and/or multifetal gestation. Reduced placental attachment sites and placental weight per fetus defined space-restricted (USR) v. control nonrestricted (NSR) fetuses. Space-restricted fetuses exhibited evidence for decreased plasma volume, with higher hematocrit and plasma albumin at gestational day (GD) 120, followed by lower blood pO2, and higher osmolarity and creatinine at GD130, P < 0.05 for all. By combining treatments, fetal kidney weight relative to fetal weight was inversely related to both fetal weight and plasma creatinine levels, P < 0.05 for both. At GD130, space-restricted fetal kidney weights, cortical depths and glomerular generations were decreased, P < 0.05 for all. Space-restricted kidneys underwent an adaptive response by prolonging active nephrogenesis and increasing maculae densa number, P < 0.05 for both. The major renal adaptations in space-restricted IUGR fetuses included immaturity in both development and endocrine function, with evidence for impaired renal excretory function.

SUBMITTER: Meyer-Gesch KM

PROVIDER: S-EPMC3805357 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Ovine fetal renal development impacted by multiple fetuses and uterine space restriction.

Meyer-Gesch K M KM Sun M Y MY Koch J M JM Ramadoss J J Blohowiak S E SE Magness R R RR Kling P J PJ

Journal of developmental origins of health and disease 20131001 5

Intrauterine growth restriction (IUGR) from uteroplacental dysfunction causes impaired nephrogenesis and ultimately hypertension, but it is unknown whether IUGR caused by insufficient space for placental development seen in uterine anomalies and/or multifetal gestation exerts the same effects. Fetal renal development and metabolism were studied in an ovine space-restriction model by combining unilateral horn surgical ligation and/or multifetal gestation. Reduced placental attachment sites and pl ...[more]

PMID: 24159370

Similar Datasets

Project description:BackgroundInvestigation of fetal cerebral maturation (FCM) is necessary and important to provide crucial prognostic information for normal and high-risk fetuses. The study aimed to develop a valid and quantitative predictive model for assessing FCM using ultrasound and validate the model for fetuses with normal and restricted growth.MethodsThis was a multicenter prospective observational study. Fetuses with normal growth recruited from a university teaching hospital (Center 1) and a municipal maternal unit (Center 2) were included in the training set and external validation set 1, respectively. The 124 growth-restricted fetuses enrolled in Center 1 were included in validation set 2. FCM was used to describe the gestational age (GA) in this study. The model was developed based on the sum of fetal cranial parameters (total fetal cranial parameters), including head circumference (HC) and depths of the insula (INS) and sylvian fissure (SF), parieto-occipital fissure (POF), and calcarine fissure (CF). A regression model, constructed based on total fetal cranial parameters and predicted GA, was established using the training set and validated using external validation set 1 and validation set 2.ResultsThe intra- and interobserver intraclass correlation coefficients for HC, and depths of the INS and SF, POF, and CF were >0.90. An exponential regression equation was used to predict FCM: predicted GA of FCM (weeks) =11.16 × exp (0.003 × total fetal cranial parameters) (P<0.001; adjusted R2=0.973), standard error of estimate, 0.67 weeks. The standard error of the predicted GA of FCM from the model was ±4.7 days. In the validation set 1, the mean standard error of the developed prediction model for FCM was 0.97 weeks. The predictive model showed that FCM was significantly delayed in validation set 2 (2.10±1.31 weeks, P<0.001), considering the GA per the last menstrual period.ConclusionsThe predictive performance of the FCM model developed in this study was excellent, and the novel model may be a valuable investigative tool during clinical implementation.

Project description:Worldwide, fetal growth restriction (FGR) affects 7%-10% of pregnancies, or roughly 20.5 million infants, each year. FGR increases not only neonatal mortality and morbidity but also the risk of obesity in later life. Currently, the molecular mechanisms by which FGR "programs" an obese phenotype are not well understood. Studies demonstrate that FGR females are more prone to obesity compared to males; however, the molecular mechanisms that lead to the sexually dimorphic programming of FGR are not known. Thus, we hypothesized that FGR leads to the sexually dimorphic programming of preadipocytes and reduces their ability to differentiate into mature adipocytes. To test the hypothesis, we utilized a maternal hyperthermia-induced placental insufficiency to restrict fetal growth in sheep. We collected perirenal adipose tissue from near-term (∼140 days gestation) male and female FGR and normal-weight fetal lambs (N = 4 to 5 in each group), examined the preadipocytes' differentiation potential, and identified differential mRNA transcript expression in perirenal adipose tissue. Male FGR fetuses have a lower cellular density (nuclei number/unit area) compared to control male fetuses. However, no difference was observed in female FGR fetuses compared to control female fetuses. In addition, the ability of preadipocytes to differentiate into mature adipocytes with fat accumulation was impaired in male FGR fetuses, but this was not observed in female FGR fetuses. Finally, we examined the genes and pathways involved in the sexually dimorphic programming of obesity by FGR. On enrichment of differentially expressed genes in males compared to females, the Thermogenesis KEGG Pathway was downregulated, and the Metabolic and Steroid Biosynthesis KEGG pathways were upregulated. On enrichment of differentially expressed genes in male FGR compared to male control, the Steroid Biosynthesis KEGG Pathway was downregulated, and the PPAR Signaling KEGG pathway was upregulated. No pathways were altered in females in response to growth restriction in perirenal adipose tissue. Thus, the present study demonstrates a sexually dimorphic program in response to growth restriction in sheep fetal perirenal adipose tissue.

Project description:Worldwide, fetal growth restriction (FGR) affects 7 to 10% of pregnancies, or roughly 20.5 million infants, each year. FGR not only increases neonatal mortality and morbidity but also the risk of obesity in later life. Currently, the molecular mechanisms by which FGR "programs" an obese phenotype are not well understood. Studies demonstrate that FGR females are more prone to obesity compared to males; however, the molecular mechanisms that lead to the sexually dimorphic programming of FGR are not known. Thus, we hypothesized that FGR leads to the sexually dimorphic programming of preadipocytes and reduces their ability to differentiate into mature adipocytes. To test the hypothesis, we utilized a maternal hyperthermia-induced placental insufficiency to restrict fetal growth in sheep. We collected perirenal adipose tissue from male and female near-term FGR and normal-weight fetal lambs (N=4 in each group, 16 total), examined the preadipocytes' differentiation potential, and identified differential mRNA transcript expression in perirenal adipose tissue. Male FGR fetuses have lower cellular density compared to control male fetuses. However, no difference was observed in female FGR fetuses compared to control female fetuses. In addition, the ability of preadipocytes to differentiate into mature adipocytes with fat accumulation was impaired in male FGR fetuses, but this was not observed in female FGR fetuses. Finally, we examined the genes and pathways involved in the sexually dimorphic programming of obesity by FGR. On enrichment of differentially expressed genes in males compared to females, the Thermogenesis KEGG Pathway was downregulated, and the Metabolic and Steroid Biosynthesis KEGG pathways were upregulated. On enrichment of differentially expressed genes in male FGR compared to male control, the Steroid Biosynthesis KEGG Pathway was downregulated, and the PPAR Signaling KEGG pathway was upregulated. No pathways were altered in females in response to growth restriction in perirenal adipose tissue. Thus, the present study demonstrates a sexually dimorphic program in response to growth restriction in sheep fetal perirenal adipose tissue.

Dataset Information

Ovine fetal renal development impacted by multiple fetuses and uterine space restriction.

Publications

Ovine fetal renal development impacted by multiple fetuses and uterine space restriction.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets