High-fat diet during mouse pregnancy impairs fetal heart development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1034047 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26617852.fastq.gz | Fastqsanger.gz | |||
| SRR26617853.fastq.gz | Fastqsanger.gz | |||
| SRR26617854.fastq.gz | Fastqsanger.gz | |||
| SRR26617855.fastq.gz | Fastqsanger.gz | |||
| SRR26617856.fastq.gz | Fastqsanger.gz |
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Project description:Maternal obesity is associated with detrimental outcomes in offspring. However, the specific effects of gestational exposure to a high-fat diet (HFD) on fetal heart development remain poorly understood. In the study, we investigated that maternal overnutrition accounted for defective development in offspring, and cell proliferation was restricted severely in neonatal organ. Starting with this clue, we found decreased cell cycle and similar cross area of cardiomyocytes in offspring exposed to a maternal HFD. Moreover, RNA sequencing analysis detected that HFD diminished fatty acid metabolism, enhanced inflammation response and up-regulated substantially the pathway TP53 regulates transcription of cell cycle genes in postnatal day 0 (P0) cardiomyocytes. Further, normal lactation after delivery not only recovered from growth retardation but also maintained normal cardiac function in offspring. These data demonstrated a potential TP53 pathway-dependent mechanism through which maternal HFD contributed to offspring cardiac defects.
2024-10-31 | GSE246648 | GEO
Project description:Maternal over- and undernutrition in pregnancy plays a critical role in fetal brain development and function. The effects of different maternal diet compositions on intrauterine programming of the fetal brain in the absence of maternal obesity or maternal undernutrition is a lesser-explored area. The goal of this study was to investigate the impact of two different maternal diets on fetal brain gene expression signatures, fetal/neonatal growth, and neonatal behavior in a mouse model. Female C57Bl/6J mice were fed one of two commercially-available chow diets (pelleted vs. powdered) with differing micronutrient and carbohydrate compositions throughout pregnancy and lactation. The powdered chow diet was richer in carbohydrates and lower in micronutrients than the pelleted chow diet, among other differences. On embryonic day 15.5, embryos were weighed and measured. Fetal brains were snap frozen. RNA was extracted from fetal forebrains for five fetuses per diet group and hybridized to whole genome expression microarrays. Functional analyses identified significant upregulation of canonical pathways and upstream regulators involved in cell cycle regulation, synaptic plasticity, and sensory nervous system development in the fetal brain, and significant downregulation of pathways related to cell and embryo death. Pathways related to DNA damage response, humoral and cell-mediated immune response, carbohydrate and lipid metabolism, small molecule biosynthesis, and amino acid metabolism were also dysregulated. Maternal dietary content is an important variable for researchers evaluating fetal brain development and offspring behavior to consider. Selection of a chow diet matched for micronutrients is crucial to avoid unexpected or undesired effects on offspring brain development and behavior.
2019-12-06 | GSE133525 | GEO
Project description:Maternal Pregnancy Diet Effect on Fetal Brain Transcriptome
| PRJNA551685 | ENA
Project description:The present study aimed to examine the effect of high-fat diet prior to pregnancy on the liver of mouse offspring. Female C57BL/6J mice were fed a normal chow (15.2% fat by energy) (CTR and CTR-PP groups) or a high-fat chow (31.2% fat by energy) (HFD and HFD-PP groups) for 3−4 weeks and then mated with male C57BL/6J mice fed normal chow. Some mothers continued on the same diet until pups reached 21 days of age (CTR and HFD), and others were fed the different chows from gestational day 0 (CTR-PP and HFD-PP) to determine the effects of a high-fat diet during the pre-pregnancy period in HFD-PP/CTR and HFD/CTR-PP comparisons. RNA sample was taken from liver of 3-week-old mouse prenatally received high-fat diet prior to pregnancy, during pregnancy and lactation, or through prior to and during pregnancy and lactation, while control RNA was taken from control counterpart prenatally received normal diet alone. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
2013-06-18 | E-GEOD-48014 | biostudies-arrayexpress
Project description:Increasing trends of obesity in childbearing women with a concurrent gestational diabetes are often associated with adverse fetal metabolic cues. Not only the carbohydrates but also fats are considered to contribute additional dietary fuels to the fetal hearts. To examine the hitherto unknown epigenetic mechanisms on the offspring’s cardiometabolic health due to maternal high-fat (HF) diet (40% kcal) or streptozotocin (STZ)-induced diabetic pregnancy, or both, we carried out an epigenetic characterization of neonatal heart tissue using chromatin immunoprecipitation (ChIP) sequening and a previously validated rat model. Chromatin landscape of offspring’s heart tissue revealed differential peaks distribution on various promoter regions mapped to the rat genome due to histone (H3) modifications by acetylation (H3Ac) or trimethylations of lysine 4 and 27 (H3K4me3 and H3K27me3, respectively). Ongoing evaluations include gene ontology and disease ontology analyses. Together, it is expected that the findings will show that maternal HF-diet with or without gestational diabetes changes the cardiac histone signature in rat offspring, potentially leading to development of novel disease prevention strategies.
2017-06-12 | GSE84831 | GEO
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment. Examination of differentially expressed genes between gestational day 15 (+/- 0.5 days) C57BL/6 mouse fetal livers from diet-induced (60% fat diet) obese or control female mice.
2014-10-25 | E-GEOD-62715 | biostudies-arrayexpress
Project description:The present study aimed to examine the effect of high-fat diet prior to pregnancy on the liver of mouse offspring. Female C57BL/6J mice were fed a normal chow (15.2% fat by energy) (CTR and CTR-PP groups) or a high-fat chow (31.2% fat by energy) (HFD and HFD-PP groups) for 3−4 weeks and then mated with male C57BL/6J mice fed normal chow. Some mothers continued on the same diet until pups reached 21 days of age (CTR and HFD), and others were fed the different chows from gestational day 0 (CTR-PP and HFD-PP) to determine the effects of a high-fat diet during the pre-pregnancy period in HFD-PP/CTR and HFD/CTR-PP comparisons.
2013-06-18 | GSE48014 | GEO
Project description:Objective Recent evidence indicates that the adult hematopoietic system is susceptible to diet-induced lineage skewing. It is not known whether the developing hematopoietic system is subject to metabolic programming via in utero high fat diet (HFD) exposure, an established mechanism of adult disease in several organ systems. We previously reported substantial losses in offspring liver size with prenatal HFD. As the liver is the main hematopoietic organ in the fetus, we asked whether the developmental expansion of the hematopoietic stem and progenitor cell (HSPC) pool is compromised by prenatal HFD and/or maternal obesity. Methods We used quantitative assays, progenitor colony formation, flow cytometry, transplantation, and gene expression assays with a series of dietary manipulations to test the effects of gestational high fat diet and maternal obesity on the day 14.5 fetal liver hematopoietic system. Results Maternal obesity, particularly when paired with gestational HFD, restricts physiological expansion of fetal HSPCs while promoting the opposing cell fate of differentiation. Importantly, these effects are only partially ameliorated by gestational dietary adjustments for obese dams. Competitive transplantation reveals compromised repopulation and myeloid-biased differentiation of HFD-programmed HSPCs to be a niche-dependent defect, apparent in HFD-conditioned male recipients. Fetal HSPC deficiencies coincide with perturbations in genes regulating metabolism, immune and inflammatory processes, and stress response, along with downregulation of genes critical for hematopoietic stem cell self-renewal and activation of pathways regulating cell migration. Conclusions Our data reveal a previously unrecognized susceptibility to nutritional and metabolic developmental programming in the fetal HSPC compartment, which is a partially reversible and microenvironment-dependent defect perturbing stem and progenitor cell expansion and hematopoietic lineage commitment.
2014-10-25 | GSE62715 | GEO
Project description:We performed RNA-seq analysis for evaluating the effect of maternal high-fructose intake on fetal brown fat development. We find that maternal high-fructose intake induces myogenic signature in fetal brown fat, indicating impairment of brown fat development by maternal high-fructose intake.
2022-01-15 | GSE193031 | GEO
Project description:Time course series of High fat diet
2010-06-09 | E-GEOD-1033 | biostudies-arrayexpress