Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112671 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gestational protein restriction is a model for low birth size. We hypothesized that taurine supplementation would protect against changes in newborn liver and muscle caused by a maternal low protein diet.
2009-11-07 | GSE12730 | GEO
Project description:Gestational protein restriction is a model for low birth size. We hypothesized that taurine supplementation would protect against changes in newborn liver and muscle caused by a maternal low protein diet. Pregnant mouse dams were subjected to different diet schemes from day 1 of pregnancy until birth. Pups were killed following birth and liver and hindleg skeletal muscle taken out and frozen at -80C until analysis. Diet schemes: Normal Protein (20% casein; NP), Normal Protein + taurine (1% taurine supplementation in water ad libitum; NP+tau), Low Protein (8% casein; LP) and LP+tau The liver and muscle samples were normalized separately.
2009-11-07 | E-GEOD-12730 | biostudies-arrayexpress
Project description:Taurine ameliorates changes occurring in newborn skeletal muscle as a result of gestational protein restriction in C57BL/6 mice, but taurine supplementation effects may be exaggerated in C57BL/6 mice due to their inherent excessive taurinuria. We examined if maternal taurine supplementation could ameliorate changes in gene expression levels, properties of mitochondria, myogenesis, and nutrient transport and sensing, in male newborn skeletal muscle caused by a maternal low protein (LP) diet in Wistar rats. LP diet resulted in an 11% non-significant decrease in birth weight, which was not rescued by taurine supplementation (LP-Tau). LP-Tau offspring had signifi-cantly lower birth weight compared to controls. Gene expression profiling revealed 895 significantly changed genes, mainly an LP-induced down-regulation of genes involved in protein translation. Taurine fully or partially rescued 32% of these changes, but with no distinct pattern as to which genes were rescued. Skeletal muscle taurine content in LP-Tau offspring was increased, but no changes in mRNA levels of the taurine synthesis pathway were observed. Taurine transporter mRNA levels, but not protein levels, were increased by LP diet. Nutrient sensing pathways were largely unaffected in LP or LP-Tau groups, although taurine supplementation caused an unexpected decrease in total Akt and AMPK protein levels. PAT4 amino acid transporter mRNA was increased by LP, and normalized by taurine supplementation. In conclusion, gestational protein restriction in rats decreased genes involved in protein translation in newborn skeletal muscle and led to changes in nutrient transporters. Taurine partly rescued these changes, hence underscoring the im-portance of taurine in development. We used microarrays to detail changes in global programme of gene expression in newborn offspring skeletal muscle brains from rats subjected to either a control diet, a low protein diet or a low protein diet + taurine supplementation
2016-10-22 | GSE89054 | GEO
Project description:Taurine is known to be important for fetal well being and to be able to prevent effects of a low birthweight phenotype when supplemented to pregnant dams. We hypothesized that gestational taurine supplementation would affect gene expression level in 4w offspring liver and skeletal muscle. Pregnant mouse dams were subjected to different diet schemes from day 1 of pregnancy until birth. Pups were killed at 4 weeks of age and liver and quadriceps skeletal muscle taken out and frozen at -80C until analysis. Diet schemes: Normal Protein (20% casein; NP), Normal Protein + taurine (1% taurine supplementation in water ad libitum; NP+tau). The liver and muscle samples were normalized separately.
2010-12-01 | E-GEOD-20577 | biostudies-arrayexpress
Project description:Gestational taurine supplementation of mice: effect on offspring gene expression in liver and skeletal muscle
| PRJNA125271 | ENA
Project description:Taurine is known to be important for fetal well being and to be able to prevent effects of a low birthweight phenotype when supplemented to pregnant dams. We hypothesized that gestational taurine supplementation would affect gene expression level in 4w offspring liver and skeletal muscle.
2010-12-01 | GSE20577 | GEO
Project description:In utero undernutrition is associated with obesity and insulin resistance, although its effect on skeletal muscle remains poorly defined. We report that, in mice, adult offspring from undernourished dams have decreased energy expenditure, decreased skeletal muscle mitochondrial content, and altered energetics in isolated mitochondria and permeabilized muscle fibers. Strikingly, when these mice are put on a 40% calorie restricted diet they lose half as much weight as calorie restricted controls. Our results reveal for the first time that in utero undernutrition alters metabolic physiology having a profound effect on skeletal muscle energetics and response to calorie restriction in adulthood. We have used a mouse model of low birth weight generated through 50% food restriction of mouse dams during the third week of gestation. We have studied in utero food restricted offspring and control offspring that were not food restricted in utero in both the ad libitum and calorie restricted states. Gene expression profiling was performed on tibialis anterior muscle from 8 mice per group, pooled in pairs.
2014-08-01 | E-GEOD-53520 | 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 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:Purpose: In this study, we used RNA-Seq to characterize differences in the Left ventricle expression profiles rats with 62-week old submited to gestational protein restricion (LP) compared to normal protein (NP) offspring during de gestacional. Methods: Total RNA was extracted from left heart (rats with 62-week old submited to gestational protein restricion (LP) (n=5) compared to normal protein (NP) offspring during de gestacional) (n=5) using the Trizol methods. RNA concentration was quantitated using the NanoDrop. A library was built for each sample, using the TruSeq Stranded mRNA kit (illumina) and submitted to sequencing. Results: By genomic sequencing analysis, we verified changes in the expression of 137 genes; After gene to gene biological evaluation and relevance, the present study demonstrated significant differences in genes linked to inflammatory activity, oxidative stress, apoptosis process, autophagy and, in hypertrophy and fibrosis pathways resulting heart function disorders. Conclusion: The present study suggests that maternal protein restriction may lead to early heart disorders in the LP offspring compared to the NP group. We may hypothesize that rapid heart dysfunction is associated with heart fibrosis, myocardial cell hypertrophy and multiple gene expression abnormalities in the LP offspring.
2021-11-17 | GSE188836 | GEO