Transcriptomic changes in the mouse brain in response to short-term high-fat metabolic stress
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941440 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23726772.fastq.gz | Fastqsanger.gz | |||
| SRR23726773.fastq.gz | Fastqsanger.gz | |||
| SRR23726774.fastq.gz | Fastqsanger.gz | |||
| SRR23726775.fastq.gz | Fastqsanger.gz | |||
| SRR23726776.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the transcriptomic changes of brain tissue by short term high fat diet. After 10 days exposing of high fat diet, whole mouse brains were extracted.
2023-03-16 | GSE226771 | GEO
Project description:Using standardized, semipurified diets is a crucial factor for reproducibility of experimental nutritional studies. For the purpose of comparability and integration of research, two European consortia, Mitofood and BIOCLAIMS, proposed an AIN-93-based standard reference diet, the standardized BIOCLAIMS low-fat diet (LFD) as well as a high-fat diet (HFD). In order to evaluate the BIOCLAIMS LFD and HFD, we performed short-term (5 days) and long-term (12 weeks) feeding experiments using male C57BL/6 mice. The HFD has the same composition as the LFD except the fat content is increased to 40% energy in exchange for carbohydrates. Both diets were accepted by the animals and proof of principle was given that the BIOCLAIMS HFD increases body weight and body fat and affects glucose homeostasis. Short-term feeding trials (5 days) were performed in order to identify metabolic and molecular parameters which can serve as acute predictors for metabolic disorders due to high-fat diet-induced obesity. We analyzed gene expression in gonadal white adipose tissue of short- and long-term fed animals with whole genome microarrays. The BIOCLAIMS HFD strongly influenced gene expression in white adipose tissue after short- and long-term intervention. A total number of 973 and 4678 transcripts were significantly different between both diets after 5 days feeding and 12 weeks feeding, respectively. A total number of 764 transcripts encoding 549 genes were significantly differentially regulated between LF and HF animals after 12 weeks feeding as well as after 5 days feeding. Of these 549 overlapping genes, a substantial number (434 genes) were expressed at a lower level and 115 genes were expressed at a higher level in the HF mice compared to the LF mice. Without exception, all genes were regulated equally. Pathway analysis revealed a prominent role for genes involved in lipid metabolism, carbohydrate metabolism and oxidative phosphorylation. This was confirmed by quantitative real-time reverse transcription PCR. The high predictive value of gene expression changes in our short-term study compared to long-term high fat feeding is a promising step to get well-defined, early biomarkers that could shorten animal trials considerably and allow a more rapid and efficient screening of different compounds. C57BL/6J wildtype male mice, aged 12 weeks, received a low-fat diet or a high-fat diet for 5 days or 12 weeks. After sacrification, white adipose tissue depots were dissected, and immediately snap frozen in liquid nitrogen. Total RNA was isolated, quantified and qualified, and subsequently used for global gene expression profiling using Agilent 4x44K microarrays.
2013-08-27 | E-GEOD-38337 | biostudies-arrayexpress
Project description:Using standardized, semipurified diets is a crucial factor for reproducibility of experimental nutritional studies. For the purpose of comparability and integration of research, two European consortia, Mitofood and BIOCLAIMS, proposed an AIN-93-based standard reference diet, the standardized BIOCLAIMS low-fat diet (LFD) as well as a high-fat diet (HFD). In order to evaluate the BIOCLAIMS LFD and HFD, we performed short-term (5 days) and long-term (12 weeks) feeding experiments using male C57BL/6 mice. The HFD has the same composition as the LFD except the fat content is increased to 40% energy in exchange for carbohydrates. Both diets were accepted by the animals and proof of principle was given that the BIOCLAIMS HFD increases body weight and body fat and affects glucose homeostasis. Short-term feeding trials (5 days) were performed in order to identify metabolic and molecular parameters which can serve as acute predictors for metabolic disorders due to high-fat diet-induced obesity. We analyzed gene expression in gonadal white adipose tissue of short- and long-term fed animals with whole genome microarrays. The BIOCLAIMS HFD strongly influenced gene expression in white adipose tissue after short- and long-term intervention. A total number of 973 and 4678 transcripts were significantly different between both diets after 5 days feeding and 12 weeks feeding, respectively. A total number of 764 transcripts encoding 549 genes were significantly differentially regulated between LF and HF animals after 12 weeks feeding as well as after 5 days feeding. Of these 549 overlapping genes, a substantial number (434 genes) were expressed at a lower level and 115 genes were expressed at a higher level in the HF mice compared to the LF mice. Without exception, all genes were regulated equally. Pathway analysis revealed a prominent role for genes involved in lipid metabolism, carbohydrate metabolism and oxidative phosphorylation. This was confirmed by quantitative real-time reverse transcription PCR. The high predictive value of gene expression changes in our short-term study compared to long-term high fat feeding is a promising step to get well-defined, early biomarkers that could shorten animal trials considerably and allow a more rapid and efficient screening of different compounds.
2013-08-27 | GSE38337 | GEO
Project description:The prevalence of the metabolic syndrome (MS) is rapidly increasing all over the world. Consequently, there is an urgent need for more effective intervention strategies. Both animal and human studies indicate that lipid oversupply to skeletal muscle can result in insulin resistance which is one of the charecteristices of the MS. C57BL/6J mice were fed a low fat (10 kcal%) palm oil diet or a high fat (45 kcal%; HF) palm oil diet for 3 or 28 days. By combining transcriptomics with protein and lipid analyses we aimed to better understand the molecular events underlying the early onset of the MS. Short-term HF-feeding led to altered expression levels of genes involved in a variety of biological processes including morphogenesis, energy metabolism, lipogenesis and immune function. Protein analysis showed increased levels of the myosin heavy chain, slow fiber type protein and the complexes II, III, IV and V of the oxidative phosphorylation. Furthermore, we observed that the main mitochondrial membrane phospholipids, phosphatidylcholine and phosphatidylethanolamine, contained more saturated fatty acids. Altogether, these results point to a morphological as well as a metabolic adaptation by promoting a more oxidative fiber type. We hypothesize that after this early adaptation, a continued transcriptional down-regulation of genes involved in oxidative phosphorylation will result in decreased oxidative capacity at a later stage. Together with increased saturation of phospholipids of the mitochondrial membrane this can result in decreased mitochondrial function which is a hallmark observed in insulin resistance and type 2 diabetes. Keywords: diet intervention and time course In the present study we investigated the short versus the long term effects of a high fat diet on the mouse muscle transcriptome by performing a genome-wide analysis of high fat diet-responsive genes. C57BL/6J mice were fed a low fat (LF) diet (10 kcal% palm oil) or a high fat (HF) diet (45 kcal% palm oil) for 3 or 28 days. Total RNA samples (n = 6 per diet per time point) were individually hybridised tot the Affymatrix mouse genome 430 2.0 array.
2007-11-30 | E-GEOD-8524 | biostudies-arrayexpress
Project description:Background
There is evidence that shifting brain metabolism with high fat and low carbohydrate diets can reduce seizure frequency in some treatment-resistant epilepsy patients, including the more flexible Modified Atkins Diet (MAD) that is more palatable, mimicking fasting and high ketone body levels. Low carbohydrate diets shift brain energy production from glycolysis to fatty acid beta-oxidation, particularly impacting neuron and astrocyte related metabolism.
Methods and findings
We evaluated the effect of short-term MAD on molecular mechanisms in surgical brain tissue from adult treatment-resistant epilepsy patients and plasma compared to Control participants consuming a non-modified higher carbohydrate diet (failure of > 2 anti-seizure medications; n = 6 MAD, mean age 43.7 years, range 21-53, diet average 10 days; n = 10 Control, mean age 41.9 years, range 28-64). There were 13 altered metabolites in plasma, including increased ketone body 3-hydroxybutyric acid, 1 metabolite in cortex, and 11 metabolites in hippocampus that were associated with mitochondrial function. Cortex and plasma 3-hydroxybutyric acid levels correlated (p = 0.0088, R2 = 0.48). Brain proteomics and RNAseq identified few differences, with trends seen in hippocampal NADH related signaling pathways (activated oxidative phosphorylation and inhibited sirtuin signaling).
Conclusions
Short-term MAD resulted in early metabolic changes in plasma and resected epilepsy brain tissue, in combination with trending changes seen in hippocampal NADH related signaling pathways. Future studies should evaluate how brain molecular mechanisms are altered with long-term MAD, with correlations to seizure frequency, epilepsy syndrome, and other clinical variables. [Clinicaltrials.gov NCT02565966]
2022-07-11 | MSV000089863 | MassIVE
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Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE229088 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE229087 | GEO
Project description:We used microarrays to unveil the gene expression alterations upon short-term HFD administration We found that short-term HFD administration impacts hepatic lipid biosynthesis and redox status
2017-08-01 | GSE94867 | GEO
Project description:Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time. The health consequences of this short-term consumption of energy-dense nutrients remain still unclear. We found that every short-term, reiterated switches to feast diets mimicking our social eating behavior, breached the potential buffering effect of the intestinal microbiota and deeply reorganized the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic, antigen-specific immunity leading to higher susceptibility to Salmonella Typhimurium and Listeria monocytogenes infections. This was explained by a reduction of CD4+ T cell metabolic fitness and cytokine production due to impaired mTOR activity in response to withdrawal of microbial provision of fiber metabolites. Reintroducing dietary fiber efficiently rewired T cell metabolism and restored both mucosal and systemic CD4+ T cell functions and immunity. Finally, dietary intervention study in human volunteers confirmed the impact of short-term dietary switches on human CD4+ T cell functionality. This work reveals that short-term nutritional changes cause a drastic yet transient depression of both mucosal and systemic immunity, creating windows of opportunities for pathogenic infections.
2023-07-11 | GSE236786 | GEO