Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA270510 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the lncRNA profiles in low birth weight rats with reduced nephron endowment induced by restriction of maternal protein intake. Low birth weight by reduced nephron endowment is a risk factor for hypertension and end-stage renal disease in adulthood.
2017-02-13 | GSE64239 | GEO
Project description:Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism. Gene expression changes in the livers of offspring exposed to alcohol in utero compared to controls.
2010-09-30 | E-GEOD-23106 | biostudies-arrayexpress
Project description:Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism. Gene expression changes in the kidneys of offspring exposed to alcohol in utero compared to controls.
2010-10-01 | E-GEOD-23105 | biostudies-arrayexpress
Project description:Maternal caloric restriction during the last week of gestation resulted in low birth weight (LBW) and increased risk of LBW-associated metabolic diseases in adult life. The metabolic phenotypes transmitted to F2 generation by paternal manner without additional altered nutrition. To investigate the mechanism of this intergenerational inheritance, two Cohorts were exposed to different magnitudes of undernutrition both in utero during the last week of gestation and/or postnatal until weaning. We performed MeDIP-seq on the genomic DNA from sperm collected from these mice.
2024-08-25 | E-MTAB-9567 | biostudies-arrayexpress
Project description:Maternal undernutrition during pregnancy followed by ad libitum access to nutrients during postnatal life induces postnatal metabolic disruptions in multiple species. As skeletal muscle is a major metabolic organ, RNAseq was performed on the longissimus dorsi muscles of slaughter-weight adult females that had been exposed to nutrient-restriction in utero.
2022-07-01 | GSE181149 | GEO
Project description:Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism.
2010-10-01 | GSE23106 | GEO
Project description:Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism.
2010-10-01 | GSE23105 | GEO
Project description:Maternal caloric restriction during the last week of gestation resulted in a low birth weight (LBW) and increased risk of LBW-associated metabolic diseases in adult life. The metabolic phenotypes transmitted to F2 generation by paternal manner without additional altered nutrition. To investigate the mechanism of this intergenerational inheritance, two Cohorts were exposed to different magnitudes of unternourition both in utero during the last week of gestation and/or post nataly until weaning. We performed small RNA-seq on non-coding RNA from sperm collected from these mice. Small RNA libraries were size-selected to be between 132 to 200 bp (including adapter) after library amplification.
2024-08-25 | E-MTAB-9565 | biostudies-arrayexpress
Project description:Low (U) and normal (N) birth weight female porcine offspring were used to study molecular and physiological changes in the liver before and after postnatal feed restriction (R, 50% of controls) and after subsequent refeeding period in comparison to non-restricted control animals (K). Overall, the following questions were addressed at the transcriptional, epigenomic and metabolic level: 1) Are there differences in the hepatic transcriptional profile between U and normal birth weight 2) Are these effects reflected on the metabolic level? 3) Could the possible birth weight-dependent effects be modified through feed restriction intervention? 4) Are these effects persistent and, moreover, can improvements with regard to lipid homeostasis be observed? Microarrays were used to study the effects of birth weight and/or feed restriction on the transcriptional level.
2016-01-23 | GSE43826 | GEO
Project description:Maternal exposure to ozone during implantation results in reduced fetal weight gain in rats. Offspring from ozone-exposed dams demonstrate sexually dimorphic risks to high-fat diet feeding in adolescence. To better understand the adolescent hepatic metabolic landscape following fetal growth restriction, RNA sequencing was performed to characterize the effects of ozone-induced fetal growth restriction on male and female offspring. Pregnant Long-Evans rats were exposed to filtered air or 0.8 ppm ozone for 4 hours on both gestation days 5 and 6 (n = 6 / group). At approximately postnatal day 48, liver tissue was obtained for RNA sequencing from offspring. Peri-implantation exposure to ozone in the dam had greater effects on hepatic gene expression in male offspring than in the females. Interestingly, heatmaps of these DEGs suggested that male offspring from ozone-exposed dams had a transcriptomic pattern like that of female offspring. Using a filtered set of highly female-predominant genes (n = 390), 57% were upregulated in the male offspring from ozone-exposed dams. Upregulated canonical pathways included sirtuin and orexin signaling, estrogen receptor signaling, and integration of energy metabolism. Relatively few genes altered in the male offspring from ozone exposed dams were associated with endpoints of sexual maturity, signifying the likely source of the observed feminization was not attributed to sex hormones. This study provides initial evidence that growth restriction in utero may increase the risk of hepatic feminization in male offspring. Additional work is needed to further understand the relationship between developmental undernutrition and feminization in the male liver.
2025-06-16 | GSE285988 | GEO