Maternal emulsifier consumption programs offspring metabolic and neuropsychological health
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE231769 | GEO | 2023/07/31
REPOSITORIES: GEO
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Project description:The specific role of nutritional status during gestation in exacerbating or mitigating fetal toxicity of ethanol (EtOH) remains unclear. We used an intragastric infusion model (Total enteral nutrition, TEN) to appropriately control for dietary EtOH consumption and caloric intake. Time impregnated female Sprague Dawley rats (250-300 g) were surgically cannulated with intragastric cannulae (on gestation day 4) and infused either control or EtOH-containing diets. Rats were fed 220 kcal/ kg3/4/d (NRC recommended caloric intake for gestation) or 160 kcal/ kg3/4/d (undernourished to 72% of control) diets containing either 12 g/kg/d EtOH or an isocaloric amount of carbohydrates from gestation days 6-15. Maternal hepatic gene expression profiles were assessed on GD15. The present data dissect specific effects of nutritional status during gestation and EtOH intake and the interaction thereof. The data reveal a highly significant interaction between undernutrition and EtOH consumption. Keywords: Nutrition-gene interactions
2006-12-03 | GSE3740 | GEO
Project description:Pregnancy is a time of extreme metabolic demand that requires coordinated adaptations between mother and fetus. To determine the contributions of maternal and fetal metabolism to metabolic plasticity during gestation, mice with a liver-specific Carnitine Palmitoyltransferase-2 knockout mice (Cpt2-/-), or Pparα KO mice were subjected to late-gestation nutrient stress, a 24hr fast from E16.5 to E17.5. The fetal response to maternal fasting was dominated by maternal lipid metabolism as the loss of maternal hepatic fatty acid oxidation or Pparα signaling accelerated fetal liver transcriptional programing. These data show that maternal nutritional environment is a major driver of perinatal metabolic programing and plasticity.
2019-09-20 | GSE129368 | GEO
Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group). 24 samples, each consisted of pooled total RNA from triplicate wells (6-well plate).
2011-12-16 | E-GEOD-34464 | biostudies-arrayexpress
Project description:It is known that both maternal and paternal health/disease can influence the early development and later metabolic homeostasis of the offspring. We investigated whether maternal exercise during gestation alone could protect the offspring from the adverse effects of either maternal or paternal obesity induced by high-fat diet (HFD). To understand the underlying mechanisms we performed transcriptomics, whole-genome DNA methylation and targeted DNA methylation analysis at the metabolic master regulator, peroxisome proliferator-activated receptor g coactivator-1a (Pgc-1a) promoter in the adult offspring skeletal muscle. Both maternal and paternal HFD resulted in impaired glucose tolerance in the offspring at 9 months of age. Maternal exercise during gestation completely mitigated this metabolic impairment induced by either maternal or paternal HFD. Adult offspring exposed to either maternal or paternal HFD without exercise during gestation had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile that was more similar to control offspring from normal chow fed parents. Changes in promoter and CpG DNA methylation were detected between the groups but did not explain the transcriptional changes. Maternal HFD increased methylation of the Pgc-1α promoter at CpG -260, which was prevented by maternal exercise. Paternal HFD did not affect the methylation of the Pgc-1α promoter. These findings demonstrate the negative consequences of maternal and paternal obesity for the offspring’s metabolic outcomes later in life and the clear benefits of maternal exercise during gestation. The mechanisms involve transcriptional regulation of skeletal muscle likely through multiple types of epigenetic modifications.
2021-07-30 | GSE144111 | GEO
Project description:It is known that both maternal and paternal health/disease can influence the early development and later metabolic homeostasis of the offspring. We investigated whether maternal exercise during gestation alone could protect the offspring from the adverse effects of either maternal or paternal obesity induced by high-fat diet (HFD). To understand the underlying mechanisms we performed transcriptomics, whole-genome DNA methylation and targeted DNA methylation analysis at the metabolic master regulator, peroxisome proliferator-activated receptor g coactivator-1a (Pgc-1a) promoter in the adult offspring skeletal muscle. Both maternal and paternal HFD resulted in impaired glucose tolerance in the offspring at 9 months of age. Maternal exercise during gestation completely mitigated this metabolic impairment induced by either maternal or paternal HFD. Adult offspring exposed to either maternal or paternal HFD without exercise during gestation had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile that was more similar to control offspring from normal chow fed parents. Changes in promoter and CpG DNA methylation were detected between the groups but did not explain the transcriptional changes. Maternal HFD increased methylation of the Pgc-1α promoter at CpG -260, which was prevented by maternal exercise. Paternal HFD did not affect the methylation of the Pgc-1α promoter. These findings demonstrate the negative consequences of maternal and paternal obesity for the offspring’s metabolic outcomes later in life and the clear benefits of maternal exercise during gestation. The mechanisms involve transcriptional regulation of skeletal muscle likely through multiple types of epigenetic modifications.
2021-07-30 | GSE144109 | GEO
Project description:Fetal alcohol exposure at any stage of pregnancy can lead to Fetal Alcohol Spectrum Disorder (FASD), a group of life-long conditions characterized by congenital malformations, as well as cognitive, behavioral, and emotional impairments. The teratogenic effects of alcohol have long been publicized; yet fetal alcohol exposure is one of the most common preventable causes of birth defects. Currently, alcohol abstinence during pregnancy is the best and only way to prevent FASD. However, alcohol consumption remains astoundingly prevalent among pregnant women; therefore, additional measures need to be made available to help protect the developing embryo before irreparable damage is done. Maternal nutritional interventions using methyl donors have been investigated as potential preventative measures to mitigate the adverse effects of fetal alcohol exposure. Here, we show that a single acute preimplantation (E2.5; 8-cell stage) fetal alcohol exposure in mice leads to long-term FASD-like morphological phenotypes (e.g., growth restriction, brain malformations, skeletal delays) in late-gestation embryos (E18.5) and demonstrate that supplementing the maternal diet with a combination of four methyl donor nutrients, folic acid, choline, betaine, and vitamin B12, prior to conception and throughout gestation effectively reduces the incidence and severity of alcohol-induced morphological defects without altering DNA methylation status and regulation of imprinting control regions. This study clearly supports that preimplantation embryos are vulnerable to the teratogenic effects of alcohol, emphasizing the dangers of maternal alcohol consumption during early gestation, and provides a potential proactive maternal nutritional intervention to minimize FASD progression, reinforcing the importance of adequate preconception and prenatal nutrition.
2023-01-23 | GSE222974 | GEO
Project description:The specific role of nutritional status during gestation in exacerbating or mitigating fetal toxicity of ethanol (EtOH) remains unclear. We used an intragastric infusion model (Total enteral nutrition, TEN) to appropriately control for dietary EtOH consumption and caloric intake. Time impregnated female Sprague Dawley rats (250-300 g) were surgically cannulated with intragastric cannulae (on gestation day 4) and infused either control or EtOH-containing diets. Rats were fed 220 kcal/ kg3/4/d (NRC recommended caloric intake for gestation) or 160 kcal/ kg3/4/d (undernourished to 72% of control) diets containing either 12 g/kg/d EtOH or an isocaloric amount of carbohydrates from gestation days 6-15. Maternal hepatic gene expression profiles were assessed on GD15. The present data dissect specific effects of nutritional status during gestation and EtOH intake and the interaction thereof. The data reveal a highly significant interaction between undernutrition and EtOH consumption. Experiment Overall Design: Four groups of time impregnated female Sprague Dawley rats were utilized. Experiment Overall Design: Group 1: Control, TEN-220, control group fed normal (non-EtOH containing) diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 2: Ethanol-220, EtOH-220 (EtOH group fed EtOH containing diets) at 12 g EtOH/kg/d diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 3: Control-160, TEN-160, (undernourished control group fed normal (non-EtOH containing) diets at 160 kcal/ kg3/4/d. Experiment Overall Design: Group 4: Ethanol-160, EtOH-160, (undernourished rats fed EtOH containing diets) at 12 g EtOH/kg/d diets at 160 kcal/ kg3/4/d
2008-06-12 | E-GEOD-3740 | biostudies-arrayexpress
Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group).
2011-12-16 | GSE34464 | GEO
Project description:Fate determination of primordial germ cells (PGCs) is regulated in a multi-layered manner, involving signaling pathways, epigenetic mechanisms and transcriptional control. Epigenetic mechanisms are expected to be closely related with metabolic mechanisms but the detailed molecular machinery linking these two layers remain poorly understood. Here, we show that the hexosamine biosynthetic pathway controls PGC fate determination via O-linked -N-acetylglucosamine (O-GlcNAc) modification. Consistent with this model, reduction of carbohydrate metabolism via a maternal ketogenic diet that decreases O-GlcNAcylation levels causes repression of PGC formation in vivo. Further, the effect of maternal ketogenic diet intake until mid-gestation affected the number of ovarian germ cells in newborn pups. Taken together, we show that nutritional and metabolic mechanisms play a previously unappreciated role in PGC fate determination.
2023-06-22 | GSE234794 | 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