Transcriptome in rat kidneys exposed to a fetal low-protein diet on postnatal days 5, 10, and 28
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE215329 | GEO | 2023/10/04
REPOSITORIES: GEO
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Project description:Maternal low-protein (MLP) diet can lead to hepatic steatosis, which only develops with ageing. It is still unclear whether the young offspring show any signs of past exposure to prenatal adverse conditions. We hypothesized that early nutritional insult would first affect the dynamic responsiveness to nutritional challenges rather than the static state. We analyzed the transcriptome and metabolome profiles of the hepatic response to fasting/refeeding in young male mice offspring to identify changes induced by early gestational MLP diet. Restricted MLP exposure strictly to early gestation was achieved by the embryo transfer method. As a result, significant transcriptional differences between control and MLP pups were found only in the fasted state. The fasting-induced upregulation of genes for long-chain fatty acid metabolism and of stress response genes related to protein folding were significantly diminished in MLP pups. Gene Set Enrichment Analysis showed that peroxisome proliferator activated receptor (PPAR)-mediated induction was impaired in fasted MLP pups. Lipid profiling showed that the hepatic signature of triacylglycerols was shifted to longer acyl-chains and higher saturation by the MLP diet. Taken together, early gestational MLP diet affected the hepatic dynamic response to nutritional stress in seemingly healthy young offspring, accompanied with partial deterioration of PPAR action.
2017-09-14 | GSE100313 | GEO
Project description:Environmental factors during perinatal development influence developmental plasticity and disease susceptibility via alterations to the epigenome. Developmental exposure to the endocrine active compound, bisphenol A (BPA), has previously been associated with altered methylation at candidate gene loci. Here, we undertake the first genome-wide characterization of DNA methylation profiles in the liver of murine offspring perinatally exposed to multiple doses of BPA through the maternal diet. Using a tiered focusing approach, our strategy proceeds from unbiased broad DNA methylation analysis using methylation-based next generation sequencing technology to in-depth quantitative site-specific CpG methylation determination using the Sequenom EpiTYPER MassARRAY platform to profile liver DNA methylation patterns in offspring maternally exposed to BPA during gestation and lactation to doses ranging from 0 BPA/kg (Ctr), 50 M-BM-5g BPA/kg (UG), or 50 mg BPA/kg (MG) diet (N=4 per group). Genome-wide analyses indicate non-monotonic effects of DNA methylation patterns following perinatal exposure to BPA, corroborating previous studies using multiple doses of BPA with non-monotonic outcomes. We observed enrichment of regions of altered methylation (RAMs) within CpG island (CGI) shores, but little evidence of RAM enrichment in CGIs. An analysis of promoter regions identified several hundred novel BPA-associated methylation events, and methylation alterations in the Myh7b and Slc22a12 gene promoters were validated. Using the Comparative Toxicogenomics Database, a number of candidate genes that have previously been associated with BPA-related gene expression changes were identified, and gene set enrichment testing identified epigenetically dysregulated pathways involved in metabolism and stimulus response. In this study, non-monotonic dose dependent alterations in DNA methylation among BPA-exposed mouse liver samples and their relevant pathways were identified and validated. The comprehensive methylome map presented here provides candidate loci underlying the role of early BPA exposure and later in life health and disease status. For this study, liver DNA from a subset of a/a wild-type animals was analyzed for full methylome characteristics: 1) standard diet (Ctr, n = 4 offspring; 2 male and 2 female); 2) 50 M-BM-5g BPA/kg diet (UG, n = 4 offspring; 2 male and 2 female); 3) 50 mg BPA/kg diet (MG, n = 4 offspring; 1 male and 3 female).
2013-11-17 | E-GEOD-46183 | biostudies-arrayexpress
Project description:It is clearly established that the maternal diet during pregnancy can induce physiological and metabolic adaptations in the developing fetus which determine its susceptibility later in life to develop diabetes, obesity... The molecular and genomic mechanisms underlying the programming of the metabolic syndrome remain largely unknown but may involve resetting of epigenetic marks and fetal gene expression. We analyzed the profile of the liver methylome in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates) during gestation and lactation. Modifications of DNA methylation were found in the promoter regions of 1,032 genes out of 14,981 genes. Bioinformatics analysis revealed that these genes are mainly involved in glucose and lipid metabolism, nervous system, coagulation, endoplasmic reticulum (ER) stress and mitochondrial function.
2015-06-22 | GSE59191 | GEO
Project description:During the last few decades, the long-lasting consequences of nutritional programming during the early phase of life have become increasingly evident, but the effects of maternal nutrition on the developing intestine are currently still relatively underexplored. In this study, we investigated in mice the effects of a maternal Western-style (WS) high fat/cholesterol diet, given during the perinatal period, on gene expression and microbiota composition of two-week-old offspring. Microarray analysis revealed that a perinatal WS diet caused significant changes in gene expression in the small intestine and colon of the suckling offspring. A strong sexually dimorphic effect was observed in the affected genes. However, pathway analysis of the differentially expressed genes displayed that in both sexes metabolic and immune functions were strongly affected. Integration of the microbiota and gene expression data applying a multivariate correlation analyses revealed that Bacteroidaceae, Porphyromonadaceae and Lachnospiraceae were the bacterial families that most strongly correlated with gene expression in the colon and not with the bacterial families displaying the most pronounced change due to perinatal exposure to a WS diet. Amongst the genes demonstrating a strong correlation with one or more bacterial families were genes of key importance for intestinal development or functioning (i.e., Pitx2 and Ace2). In conclusion, our data demonstrate a strong programming effect of a maternal WS diet on the development of the intestine in the offspring. Small intestine and colon were isolated from two-week-old pups of dams fed a low- or Western-style high fat/cholesterol diet and subjected to gene expression profiling.
2016-08-22 | E-GEOD-72705 | biostudies-arrayexpress
Project description:It is clearly established that the maternal diet during pregnancy can induce physiological and metabolic adaptations in the developing fetus which determine its susceptibility later in life to develop diabetes, obesity... The molecular and genomic mechanisms underlying the programming of the metabolic syndrome remain largely unknown but may involve resetting of epigenetic marks and fetal gene expression. We analyzed the profile of the liver methylome in 21-day-old rats born to mothers fed with a standard diet or a diet lacking methyl donor nutrients (Vitamin B12 and folates) during gestation and lactation. Modifications of DNA methylation were found in the promoter regions of 1,032 genes out of 14,981 genes. Bioinformatics analysis revealed that these genes are mainly involved in glucose and lipid metabolism, nervous system, coagulation, endoplasmic reticulum (ER) stress and mitochondrial function. MDD induced modifications of methylation in rat liver were measured in 21-day-old rats born to dams fed with standard food or food deficient in methyl group donor. Six independent experiments were performed (3 controls versus 3 MDD).
2015-06-22 | E-GEOD-59191 | biostudies-arrayexpress
Project description:Early nutritional environment affects development and long-term health. Our objective was to determine the effect of maternal high fat diet (HFD) during pregnancy and lactation on neonate`s duodenum histomorphology and proteome. Female mice were fed either a control diet (10% kcal fat; C) or a HFD (60% kcal fat) for four weeks, and bred. On postnatal day 2, litters were standardized to ten pups and half the pups were cross-fostered to dams fed on different diets, creating four treatment combinations: C-C (control), C-HF, HF-C, HF-HF. On postnatal day 12, pups` duodenum were excised and prepared for histology and LC-MS/MS analysis of proteome. Villi were significantly longer in duodenum of HF-HF pups compared to all other treatments. However, crypt cell proliferation rate was not different among treatments. Over 3000 proteins were detected, with 1054 commonly expressed across all groups. Between control and HF-HF, HF-C or C-HF, 812, 601 or 894 proteins were differentially expressed (Tukey adj-P <0.05), respectively. Functional analysis clustered proteins upregulated in HF-HF versus control in fat digestion and absorption, extracellular matrix, cell adhesion, immune response, oxidation-reduction processes, phagocytosis and transport categories. Proteins downregulated were classified as RNA splicing, translation, protein folding, endocytosis and transport. Thus the effect of nutritional environment on intestinal tract structure and function is manifested as early as postnatal day 12. In particular, exposure to maternal HFD during pregnancy and lactation changed fat digestion and absorption processes, increased extracellular matrix and focal adhesion proteins, and heightened innate and active immune response.
2018-08-28 | MSV000082860 | MassIVE
Project description:Genetic and environmental factors interact during sensitive periods early in life to influence mental health and disease via epigenetic processes such as DNA methylation. However, it is not known if DNA methylation changes outside the brain provide an 'epigenetic signature' of early-life experiences. Here, we employed a novel intra-individual approach by testing DNA methylation from buccal cells of individual rats before and immediately after exposure to one week of typical or adverse life experience. We find that whereas inter-individual changes in DNA methylation reflect the effect of age, DNA methylation changes within paired DNA samples from the same individual reflect the impact of diverse neonatal experiences. Genes coding for critical cellular–metabolic enzymes, ion channels and receptors were more methylated in pups exposed to the adverse environment, predictive of their repression. In contrast, the adverse experience was associated with less methylation on genes involved in pathways of death and inflammation as well as cell-fate related transcription factors, indicating their potential upregulation. Thus, intra-individual methylome signatures indicate large-scale transcription-driven alterations of cellular fate, growth and function.
2019-03-23 | GSE119640 | GEO
Project description:Nutritional imbalances in the early developmental period have an impact on the long-term risk of developing non-alcoholic fatty liver disease (NAFLD). In the present study, we demonstrated that tauroursodeoxycholic acid (TUDCA), a secondary bile acid, and markedly ameliorated hepatic steatosis in a mouse model of undernourishment in utero. Herein, we studied the effect of maternal caloric restriction on genetic expression by microarray analysis among 3 different time points of independent cohorts. Cohort 1 (at 9 weeks; without HFD), cohort 2 (at 17 weeks; with HFD), and cohort 3 (at 22 weeks; HFD with or without the TUDCA treatment) (Muramatsu-Kato et al., 2015). We compared the alteration in gene expression between NN pups and UN pups before and after postnatal high-fat diet (HFD) at 9 weeks and 17 weeks. Later we studied the TUDCA treatment responce on NN pups and UN pups.
2019-11-19 | GSE123733 | GEO
Project description:Children born to diabetic and obese or overweight mothers have a higher risk of heart disease at birth and later in life. Our previous work using chromatin immunoprecipitation sequencing revealed that late-gestation diabetes in combination with maternal high fat diet causes a distinct fuel-mediated epigenetic reprogramming of cardiac tissue during fetal cardiogenesis. We used gene expression profiling to investigate the overall transcriptional signature of newborn rat offspring exposed to the combination of maternal diabetes and maternal high fat diet.
2020-09-02 | GSE150649 | GEO
Project description:Calorie restriction (CR) has been shown to extend life- and health-span in model species. For most humans, a life-long CR diet is too arduous to adhere to. The aim of this study was to explore whether weekly intermittent CR can 1) provide long-term beneficial effects and 2) counteract diet-induced obesity in male aging mice. In this study, we have exposed C57Bl/6J mice for 24 months to an intermittent (INT) diet, alternating weekly between CR of a control diet and ad libitum moderate-fat (MF) feeding. This weekly intermittent CR significantly counteracted the adverse effects of the MF diet on mortality, body weight and liver health markers in male 24-month-old mice. Hepatic gene expression profiles of INT-exposed animals appeared much more comparable to CR than to MF-exposed mice. At 12 months of age, a subgroup of MF-exposed mice was transferred to the INT diet. Gene expression profiles in the liver of the 24-month-old diet switch mice were highly similar to the INT-exposed mice. However, a small subset of genes was consistently changed by the MF diet during the first phase of life. Weekly intermittent CR largely, but not completely, reversed adverse effects caused by a MF diet.
2017-01-16 | GSE93642 | GEO