Expression Data from Young Uteroplacental Insufficiency-induced Low Birth Weight Adult Guinea Pig Offspring
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PROVIDER: PRJNA675617 | ENA |
REPOSITORIES: ENA
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Project description:We aimed to gain mechanistic insights into the impact of uteroplacental insufficiency upon hepatic cholestrol metabolism pathways in young adult offspring.Uterine artery ablation-induced low birth weight (LBW) and normal birth weight (NBW) male and female guinea pig offspring were fed a control diet from weaning until postnatal day 150. Analysis of whole hepatic transcriptome results identified that between LBW and NBW offspring livers, 51 (29 up-regulated and 22 down-regulated) and 31 (8 up-regulated and 23 down-regulated) genes were differentially expressed in males and females respectively (fold change| >= 2 and p-value < 0.05). KEGG pathway analysis of these differentially expressed genes revealed that “Cholesterol metabolism” was an enriched pathway in LBW males but not females (p<0.05).
2020-11-10 | GSE161124 | GEO
Project description:Maternal effects on offspring phenotype do not end at birth. Bioactive factors are transmitted from mother to nursing offspring through colostrum, which is known as lactocrine programming. The lactocrine hypothesis posits that disruption of lactocrine signaling from birth will have both short- and long-term effects on the postnatal developmental program with lasting consequences. Previous research established that lactocrine insufficiency from birth in pigs, indicated by reduced serum immunoglobulin immunocrit (iCrit) ratios in nursing piglets on the day of birth (postnatal day 0, PND0), altered the postnatal uterine developmental program and reduced lifetime fecundity in adult, neonatally lactocrine insufficient females. To determine the effects of lactocrine insufficiency on uterine development in the rapid growth phase, we performed RNA sequencing in six high-low iCrit pairs in PND14 gilt littermates. High-quality RNA-seq reads were mapped to the porcine reference genome, and the expression levels were quantified in the uterus transcriptome. We identified 148 (1.1% of expressed genes) differentially expressed genes (DEGs) between the high and low iCrit groups at P < 0.05, including the the FOXA2 gene, which was known to be downregulated in low-iCrit uterus samples. Gene ontology analysis reveals that immune-related functions, including the complement pathways are up-regulated in the low iCrit group.
2022-11-08 | GSE179830 | GEO
Project description:We explored the hypothesis that gene expression will be dysregulated in the liver of low birth weight (LBW) offspring, distinct from normal birth weight (NBW) offspring, in young adulthood when both birth weight outcomes are challenged with a lifelong postnatal Western diet (WD). Independent of diet, in LBW vs. NBW males, 7 differentially expressed genes (DEGs) were identified, most of which downregulated (5 vs. 2) in LBW males. A similar trend was observed in LBW vs. NBW females, where 12 DEGs were identified, predominantly downregulated in the LBW group (9 vs. 3), irrespective of diet. Lifelong WD consumption exerted a marked influence on liver transcription profiles. Notably, 553 (444 upregulated and 109 downregulated) and 639 (533 upregulated and 106 downregulated) DEGs were identified in males and females, independent of birth weight, respectively. Additionally, in females, birth weight and WD both impacted six genes. Further, transcriptomic analysis revealed 22 (9 upregulated and 13 downregulated) and 55 (12 upregulated and 43 downregulated) DEGs between LBW/WD and NBW/WD groups in males and females, respectively.
2024-09-16 | GSE276971 | GEO
Project description:Epigenetic profiling of birth-weight discordant twins using Illumina's 450K Human DNA methylation BeadChip Comparing DNA methylation difference in birth-weight discordant twin pairs
2014-12-15 | E-GEOD-61496 | biostudies-arrayexpress
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model. Epididymal fat samples were obtained at age 3 weeks from 5 control mice (CC), 5 mice exposed to in utero undernutrition (UC), and 4 mice exposed to undernutrition in utero and during suckling (UU).
2010-03-04 | E-GEOD-16083 | biostudies-arrayexpress
Project description:16S rRNA gene sequencing of the extremelly birth weight infant gut
| PRJEB17882 | ENA
Project description:Sub-optimal fetal development is associated with an increased risk of developing cardiovascular disease, type 2 diabetes (T2D) and adiposity later in life. However, definitions of intrauterine growth restriction (IUGR) and small for gestational age (SGA) are based on simple statistical approaches that may misclassify infants with a normal developmental profile and vice versa. We used an unbiased global profiling approach to identify gene expression patterns in umbilical cord tissue from 38 infants and identified a set of 466 genes which separated the subjects into 2 distinct groups – one biased towards lower birth weight and one biased towards normal birth weight. The data suggest that approximately 30% of children of normal size have a molecular profile more typical of impaired fetal development and who may be on a programmed trajectory. Differences in expression between the two groups encompassed 384 upregulated and 82 downregulated genes. Molecular profiling at birth may have utility in identifying markers that potentially reflect antenatal developmental and may be predictive of future phenotypic development after birth. Importantly, it may provide an alternative to the current classification of infants using birth weights. RNA from umbilical cord tissue from full term neonates was extracted and hybridized. Separation into 2 distinct groups, independent of birth weight, but based solely on gene expression levels was analysed by Genespring. After appropriate statistical analysis, one group was keenly associated with a higher birth weight (22 samples) while the other was associated with a lower birth-weight (18 samples). Technical replicates were included for all 40 samples.
2011-10-20 | E-GEOD-24818 | biostudies-arrayexpress
Project description:Epigenetic profiling of birth-weight discordant twins using Illumina's 450K Human DNA methylation BeadChip
2014-12-15 | GSE61496 | GEO
Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is unexplored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>
2024-02-12 | MTBLS1629 | MetaboLights
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model.
2009-05-14 | GSE16083 | GEO