Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1129137 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29621900_1.fastq.gz | Fastqsanger.gz | |||
| SRR29621900_2.fastq.gz | Fastqsanger.gz | |||
| SRR29622000_1.fastq.gz | Fastqsanger.gz | |||
| SRR29622000_2.fastq.gz | Fastqsanger.gz | |||
| SRR29621901_1.fastq.gz | Fastqsanger.gz |
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Project description:This study examined gene expression in liver, fat and skeletal muscle of juvenile baboons to determine the effect of maternal under-nutrition (MUN; dams were fed a diet with 30% reduction in nutrients) during pregnancy on response to consumption of a high-fat, high-carbohydrate, high-salt and sugar drink (HFCS) diet for 7 weeks later in development of MUN offspring. After dietary challenge, gene expression in the liver, fat and skeletal muscle of MUN juvenile baboons was compared with that of control juvenile baboons (CON; dams were fed a control diet). Results showed that the number of differentially expressed genes and enriched pathways in these tissues differed between MUN and CON juvenile baboons.
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Project description:Purpose: NGS was used to determine if a distinct transcriptomic profile is observed among the experimental mice fed four different dietary components. Methods: We carried out RNA-Seq analysis of ileum tissue from 6 weeks male mice ad libitum fed for 10 weeks a high liquid sugar (23% (w/v)) or/and high fat (60% Kcal from fat) diet. The combined effect of sugar drink and high fat diet (HF-Sugar) was compared with sugar drink only (NF-Sugar), or high fat diet only (HF), or control diet that was plain water and normal fat diet (NF). Results: RNA-Seq revealed sample-specific clusters that included genes responding to each experimental diet. We found only addition of sugar drink to high fat group (HF-Sugar) not NF-Sugar and HF, there was a significant enrichment in biological functions relating to Inflammatory/Immune Responses, especially including dendritic cell (DC) and T cell related signaling pathway. Conclusions: Taken together, our data demonstrate that sugar drink synergistically promotes and exacerbates inflammatory responses driven by the high fat diet.
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Project description:Maternal overnutrition increases inflammatory and metabolic disease risk in postnatal offspring. This constitutes a major public health concern due to the increasing prevalence of these diseases yet the mechanisms remain unclear. Here, using nonhuman primate models, we show that maternal Western-style diet (mWSD) exposure is associated with persistent pro-inflammatory phenotypes at the transcriptional, metabolic, and functional levels in bone marrow-derived macrophages (BMDMs) from 3-year-old juvenile offspring and in hematopoietic stem and progenitor cells (HSPCs) from fetal and juvenile bone marrow and fetal liver. mWSD exposure is also associated with increased oleic acid in fetal and juvenile bone marrow and fetal liver. ATAC-seq profiling of HSPCs and BMDMs from mWSD-exposed juveniles supports a model in which HSPCs transmit pro-inflammatory memory to myeloid cells beginning in utero. These findings demonstrate that maternal diet alters long-term immune cell developmental programming in HSPCs with proposed consequences for chronic diseases featuring altered immune/inflammatory activation across the lifespan.
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Project description:A high-sugar diet induces lifestyle-associated metabolic diseases, such as obesity and diabetes, which may underlie the pro-tumor effects of a high-sugar diet. We supplied GL261 syngeneic glioblastoma (GBM) model mice with a short-term high-glucose diet (HGD) and found an increased survival rate with no evidence of metabolic disease. Modulation of the gut microbiota by an HGD was critical for enhancing the anti-tumor immune response. Single-cell RNA sequencing showed that modulation of the gut microbiota by an HGD increased the T cell-mediated anti-tumor immune response in GBM mice. We found that the cytotoxic CD4+ T cell population in GBM mice increased due to synergy with anti-PD-1 immune checkpoint inhibitors, but this depended on an HGD. Thus, we determined that an HGD enhanced anti-tumor immune responses in GBM mice through changes in the gut microbiota and suggest that the role of an HGD in GBM should be re-examined.
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Project description:Maternal obesity is a growing health concern that predisposes offspring to metabolic dysfunction, immune system alterations, and neurodegenerative disorders. To investigate the intergenerational effects of maternal obesity, we used Drosophila melanogaster models exposed to high-sugar (HSD) and high-fat diets (HFD). We found that maternal diet-induced obesity significantly altered offspring lifespan, immune function, and neuronal health in a sex- and diet-specific manner. Male offspring were particularly susceptible, exhibiting reduced lifespan, impaired climbing ability, and increased axonal degeneration, especially following maternal HFD exposure. Transcriptomic analyses revealed age-dependent and diet-specific changes, with males showing pronounced alterations at 50 days of age. Developmental programming of hemocytes (macrophage-like cells) played a crucial role in these outcomes, as knockdown of key immune pathways such as Relish and Upd3 in hemocytes further influenced lifespan in a diet-specific manner. These findings highlight the complex interplay between maternal diet and immune function, underscoring the importance of immune cells in mediating the long-term health consequences of maternal obesity. Our study provides new insights into conserved mechanisms linking maternal metabolic health to offspring outcomes and emphasizes the continued need for animal models to understand intergenerational health impacts.
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