Expression Data from Young Uteroplacental Insufficiency-induced Low Birth Weight Adult Guinea Pig Offspring
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ABSTRACT:
ORGANISM(S): Cavia porcellus
PROVIDER: GSE161124 | GEO | 2020/11/10
REPOSITORIES: GEO
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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: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
Project description:Analysis of gene expression in the lungs of pigs from high and low litter birth weight groups (HBW and LBW) inoculated with swine influenza virus. The aim of the experiment is to determine whether litter birth weight has an effect on the innate immune response to infection in pigs, and whether differences in gene expression can be linked to epigenetic differences between the two birth weight groups. A two condition experiment: lung tissue RNA from HBW and LBW SIV-infected pigs. 16 biological replicates for each condition, each hybridized with a reference to separate arrays. 32 arrays in total.
2015-10-27 | E-GEOD-62765 | biostudies-arrayexpress
Project description:Poor maternal nutrition causes intrauterine growth restriction (IUGR); however, its effects on fetal cardiac development are unclear. We have developed a baboon model of moderate maternal undernutrition, leading to IUGR. We hypothesized that the IUGR affects fetal cardiac structure and metabolism. Six control pregnant baboons ate ad-libitum (CTRL)) or 70% CTRL from 0.16 of gestation (G). Fetuses were euthanized at C-section at 0.9G under general anesthesia. Male but not female IUGR fetuses showed left ventricular fibrosis inversely correlated with birth weight. Expression of extracellular matrix protein TSP-1 was increased (p<0.05) in male IUGR. Expression of cardiac fibrotic markers TGFß, SMAD3 and ALK-1 were downregulated in male IUGRs with no difference in females. Autophagy was present in male IUGR evidenced by upregulation of ATG7 expression and lipidation LC3B. Global miRNA expression profiling revealed 56 annotated and novel cardiac miRNAs exclusively dysregulated in female IUGR, and 38 cardiac miRNAs were exclusively dysregulated in males (p<0.05). Fifteen (CTRL) and 23 (IUGR) miRNAs, were differentially expressed between males and females (p<0.05) suggesting sexual dimorphism, which can be at least partially explained by differential expression of upstream transcription factors (e.g. HNF4a, and NF?B p50). Lipidomics analysis of fetal cardiac tissue exhibited a net increase in diacylglycerol and plasmalogens and a decrease in triglycerides and phosphatidylcholines. In summary, IUGR resulting from decreased maternal nutrition is associated with sex-dependent dysregulations in cardiac structure, miRNA expression, and lipid metabolism. If these changes persist postnatally, they may program offspring for higher later life cardiac risk.
2018-04-30 | MTBLS426 | MetaboLights
Project description:Low Birth Weight (LBW) newborns (with weight less than 2500g) suffer a higher frequency and severity of microbial infection than normal birth weight (NBW) newborns. Morbidity and mortality of LBW infants due to infectious diseases are known to be high and it has been associated with compromised immune functions, however, the complete understanding of the cause is lacking. We, therefore, conducted a gene expression study to identify all the defective pathways and functions in the LBW newborns using DNA microarray. RNA were isolated from the umbilical cord blood of the NBW and LBW newborns and processed for chip hybridisation. Our results suggest down-regulation of genes participating in several canonical pathways vital in the defense response against microbes and perpetuation of immune responses. Pattern recognition receptors (PRRs) and Interferon signaling appear to be most significantly impacted pathways. The information generated from this study may help in depth understanding of the cause of higher frequency of infections in LBW and thus, in turn help devise better therapeutic interventions.
2012-01-15 | GSE29807 | GEO
Project description:Low Birth Weight (LBW) newborns (with weight less than 2500g) suffer a higher frequency and severity of microbial infection than normal birth weight (NBW) newborns. Morbidity and mortality of LBW infants due to infectious diseases are known to be high and it has been associated with compromised immune functions, however, the complete understanding of the cause is lacking. We, therefore, conducted a gene expression study to identify all the defective pathways and functions in the LBW newborns using DNA microarray. RNA were isolated from the umbilical cord blood of the NBW and LBW newborns and processed for chip hybridisation. Our results suggest down-regulation of genes participating in several canonical pathways vital in the defense response against microbes and perpetuation of immune responses. Pattern recognition receptors (PRRs) and Interferon signaling appear to be most significantly impacted pathways. The information generated from this study may help in depth understanding of the cause of higher frequency of infections in LBW and thus, in turn help devise better therapeutic interventions. Total 12 subjects were included in the study. 4 NBW newborns umblical cord blood samples served as control and 8 LBW newborns umblical cord blood samples were treated as the experimental samples for the study.
2012-01-15 | E-GEOD-29807 | biostudies-arrayexpress
Project description:Expression Data from Young Uteroplacental Insufficiency-induced Low Birth Weight Adult Guinea Pig Offspring
| PRJNA675617 | ENA
Project description:Background: Assisted Reproductive Technologies (ART) - treatments to allow parenthood to couples facing fertility issues- have allowed the birth of > 5 million babies worldwide. Notwithstanding most of ART children are healthy at birth, several studies reported that ART may affect early-life experience causing permanent changes in fetal programming and, consequently, leading to increased predisposition to metabolic disorders in adulthood. Currently, the metabolic health status of ART children has been poorly investigated and it will take decades before large-scale population studies will be implemented. Studies on animal models indicated impaired in utero development of ART conceptuses. Relevantly, our preliminary data showed hypomethylation of liver from ART foetuses, which may contribute to the fetal programming of adult diseases. Regarding adult ART offspring, obesity, glucose intolerance and lipid accumulation in the liver have been previously described in mouse model, indicative of increased risk to develop metabolic disorders. However, little is known on the pathophysiological mechanism behind the metabolic abnormalities in ART offspring. In this context, this study investigated the influence of ART on the function of the liver, a major organ involved in the maintenance of metabolic homeostasis.
Methods: To assess the influence of ART on liver functions, proteomic analysis was carried out on adult liver from 4 months old offspring developed following Embryo Transfer (ET), in vitro culture (IVC) and blastomere biopsy (BB). Control (CTR) consisted of naturally conceived offspring. Then, to verify whether and how changes in liver proteome were associated with perturbation of the metabolic status of adult offspring, general growth and physiological parameters (e.g. glucose tolerance, insulin resistance, plasmatic levels of interleukin 6, triglycerides and total cholesterol) were assessed.
Results: Proteomic analysis of adult liver showed deregulated expression of proteins involved in lipid, carbohydrate and energy metabolism as well as cellular processes in adult offspring developed following BB, IVC and ET. Characterization of metabolic phenotype of adult offspring revealed increased body weight in ART offspring, glucose intolerance in BB, IVC, ET males and BB females, insulin resistance on BB offspring, low plasmatic level of Interleukin-6 in BB, IVC, ET males and high level of triglycerides and total cholesterol in BB females vs CTR which are phenotypic manifestation of liver disfunctions and core symptoms of metabolic syndrome.
Conclusion: Our study showed DE of proteins involved in metabolic and cellular processes, indicative of impaired hepatic functions which may contribute to the onset and progression of various diseases (e.g. NASH, NAFLD, hepatocarcinoma) in mouse offspring developed following ART. Moreover, impaired hepatic metabolism was associated with obesity, glucose intolerance, insulin resistance and dyslipidaemia which are core symptoms of metabolic syndrome and risk factor for diabetes and cardiovascular diseases in adult ART offspring. Thus, we provide evidence of Assisted Reproductive Technologies is a risk factor for perturbation of hepatic proteome, associated with the increased predisposition to liver diseases and metabolic syndrome in adulthood.
2020-05-14 | MSV000085413 | MassIVE
Project description:Analysis of gene expression in the lungs of pigs from high and low litter birth weight groups (HBW and LBW) inoculated with swine influenza virus. The aim of the experiment is to determine whether litter birth weight has an effect on the innate immune response to infection in pigs, and whether differences in gene expression can be linked to epigenetic differences between the two birth weight groups.
2015-10-27 | GSE62765 | GEO
Project description:In rainbow trout (Oncorhynchus mykiss), the effect of a paternal and a maternal "high carbohydrate/low protein" diet was assessed on progeny. To this purpose, two-year old males and females rainbow trout were fed either a control diet or a "high carbohydrate/low protein" diet for an entire reproductive cycle for females and for 5 months for males. Crossed-fertilizations were carried out in order to obtain 4 groups of offspring. Offspring were fed with a commercial diet until they reached a market size. At this stage, hepatic transcriptomes were compared to detect any impact of the parental diet on offspring metabolism.
2021-08-16 | GSE169001 | GEO