RNA-sequencing data of liver tissue of intrauterine growth restricted (IUGR) piglets with or without supplementary energy treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE226052 | GEO | 2023/03/01
REPOSITORIES: GEO
Similar Datasets
Project description:Breast milk has shown neurodevelopmental advantages compared to infant formula, especially in IUGR infants, which may relate to the fat source. This study aimed to compare neurodevelopmental outcomes in normal birth weight (NBW) and intrauterine growth restricted (IUGR) piglets fed a formula diet with either a vegetable oil (VEG) or bovine milk fat source (MILK). Results showed that total plasma lipids were increased by feeding the MILK diet. 82% and 11% of lipid species were differentially expressed between dietary groups in plasma and hippocampus, respectively, with slight agreement between the plasma and brain lipidome. The MILK diet was most effective in increasing brain lipid accretion, mainly comprising phospholipids. Absolute regional brain weights, grey and white matter volumes, and behavior and motor function scores were lower in IUGR piglets with no effects of diet. Cognitive function and gene expression profiles were similar for dietary and weight groups, and overall only minor interactive effects between diet and weight were observed. In conclusion, dietary fat source influenced the plasma and to a lesser degree the hippocampal lipidome, but was unable to improve on IUGR induced brain structural and functional impairments.
2022-02-16 | GSE182263 | GEO
Project description:Intrauterine growth restriction (IUGR) is associated with increased relative liver weight at birth, hepatic function decline, and a higher risk for chronic liver and cardiovascular diseases in adults. Precise mechanisms of early developmental plasticity to intervene in poor fetal programming and adult disease remain largely elusive and warrant extensive research. Selecting natural piglets’ model of IUGR, using the liver as a readout and combining previous transcriptome findings, a map of cellular landscape was created to reveal a sex-dependent manner in IUGR-induced hepatic injury and its long-term functional repercussions.Here, we show data on the transcriptional profiles of 41,969 high-quality cells from normal birthweight (NBWs) and IUGR piglets (IUGRs) from hepatic tissue and demonstrated strong homology with human using human-derived liver single-cell dataset. We discovered that male liver was much more severely damaged and inflammation by IUGR than female liver at the one-week postnatal node.
2024-01-31 | GSE222949 | GEO
Project description:Intrauterine growth restriction (IUGR) impairs fetal growth and development, perturbs nutrient metabolism, and increases the risk of developing diseases in the postnatal life. However, the underlying mechanisms by which IUGR affects fetuses remain incompletely understood. Here, we applied high-throughput proteomics approach and biochemical analysis to investigate the impact of IUGR on fetal liver.
2016-03-15 | PXD003524 | Pride
Project description:Comparison of distal small intestine and colon in IntraUterine Growth Restricted versus normal birth weight piglets at the age of 19 days of life. Keywords: Nutritional state comparative analysis.
2010-01-01 | GSE14716 | GEO
Project description:Comparison of distal small intestine in IntraUterine Growth Restricted piglets fed either adequate or high protein artificial milks during suckling period. Comparison at 7 and 28 days of life. Keywords: Nutritional response
2010-01-01 | GSE18249 | GEO
Project description:Comparison of distal small intestine and colon in IntraUterine Growth Restricted versus normal birth weight piglets at the age of 19 days of life. Keywords: Nutritional state comparative analysis. 22 samples - One sample versus a pool
2010-05-16 | E-GEOD-14716 | biostudies-arrayexpress
Project description:Intrauterine growth restriction (IUGR) is associated with increased relative liver weight at birth, hepatic function decline, and a higher risk for chronic liver and cardiovascular diseases in adults. Precise mechanisms of early developmental plasticity to intervene in poor fetal programming and adult disease remain largely elusive and warrant extensive research. Selecting natural piglets’ model of IUGR, using the liver as a readout and combining previous transcriptome findings, a map of cellular landscape was created to reveal a sex-dependent manner in IUGR-induced hepatic injury and its long-term functional repercussions.Here, we show data on the transcriptional profiles of 41,969 high-quality cells from normal birthweight (NBWs) and IUGR piglets (IUGRs) from hepatic tissue and demonstrated strong homology with human using human-derived liver single-cell dataset. We discovered that male liver was much more severely damaged and inflammation by IUGR than female liver at the one-week postnatal node.
2024-01-31 | GSE233802 | GEO
Project description:Comparison of distal small intestine in IntraUterine Growth Restricted piglets fed either adequate or high protein artificial milks during suckling period. Comparison at 7 and 28 days of life. Keywords: Nutritional response 22 samples - One sample versus a pool
2010-05-16 | E-GEOD-18249 | biostudies-arrayexpress
Project description:Impaired muscle growth as a result of IUGR is a major contributor to lifelong reductions in muscle mass (sarcopenia) and metabolic disease risk. We use an ovine model of chronic placental insufficiency which restricts nutrient supply from mother to fetus and results in intrauterine growth restriction. In our model of placental insufficiency and IUGR, fetal hindlimb muscles weigh less than normally-grown control fetuses and have smaller myofiber diameters. Given the frequent correlation between functional changes and transcriptional changes, we investigated the effect of chronic placental insufficiency and IUGR on fetal skeletal muscle gene expression. We found that gene expression in the skeletal muscle is significantly altered by chronic placental insufficiency. In gene ontology analysis, we found that genes involved in cell cycle regulation were most significantly affected, with downregulation of several cyclins. These observations may in part account for decreased muscle weight relative to brain weight observed in the late gestation IUGR fetus.
2014-12-31 | GSE64578 | GEO
Project description:Perturbations of the intrauterine environment can affect fetal development during critical periods of plasticity, and can increase susceptibility to a number of age-related diseases (e.g. type 2 diabetes mellitus; T2DM), manifesting sometimes decades later. We hypothesized that this biological memory is mediated by permanent alterations of the epigenome in stem cell populations. Our studies focused specifically on DNA methylation in CD34+ hematopoietic stem and progenitor cells from cord blood, and utilized a two-stage design involving genome-wide discovery followed by quantitative, single-locus validation. We found that changes in cytosine methylation occur in response to intrauterine growth restriction (IUGR), but that they are of a substantially lesser degree and involve many fewer loci than the epigenomic dysregulation observed in cancer. This is consistent with a comparable study of individuals born following maternal starvation during the Dutch famine. We also identify specific loci that are targeted for dysregulation of DNA methylation, in particular the hepatocyte nuclear factor 4α (HNF4A) gene, a well-known diabetes candidate gene not previously associated with growth restriction in utero, and other loci encoding HNF4A-interacting proteins. Our results give some insights into the potential contribution of epigenomic dysregulation in mediating the long-term consequences of IUGR, and demonstrate the value of this approach to studies of the fetal origin of adult disease. Direct comparison of DNA methylation in 10 neonatal CD34+ samples isolated from umbilical cord blood belonging to two groups: IUGR (n=5) and their age-matched controls (n=5). Each microarray consists of a two-color comparison of a methylation-sensitive representation of the genome (HpaII) with an internal methylation-insensitive control/reference (MspI).
2010-02-17 | E-GEOD-17727 | biostudies-arrayexpress