Intermittent fasting alters the spatiotemporal atlas of transcriptomes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE154797 | GEO | 2022/10/27
REPOSITORIES: GEO
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Project description:Intermittent fasting is previously reported to exhibit neuroprotection against experimental ischemic stroke. However, the detailed understanding of protection mechanisms are lacking. By observing the overall transcriptomic changes in each timepoint of ischemic stroke would benefit the understanding of underlying active pathways and mechanisms. Here, we conduct experimental MCAO ischemic stroke on mice exposed to different daily intermittent fasting method to compare not only among the ischemic stroke timepoints but also the efficacy of different intermittent fasting interventions. Our current study presented the transcriptomic changes for the first time in specific timepoints of ischemic stroke as well as under the condition of intermittent fasting. A number of neuroprotective mechanisms-related genes were significantly affected by intermittent fasting conditions in differential manners.
2018-07-11 | GSE116878 | GEO
Project description:In obesity, sustained adipose tissue (AT) inflammation constitutes a cellular memory that limits the effectiveness of weight loss interventions. Yet, its fasting regimen-dependent regulation is unknown. Here, we show that cyclic intermittent fasting (IF) exacerbates the lipid-associated macrophage (LAM) inflammatory phenotype of visceral AT in obese mice. Importantly, we provide evidence that this increase in LAM abundance is almost entirely dependent on p53-driven adipocyte apoptosis. Adipocyte-specific deletion of p53 prevents LAM accumulation in AT during IF and increases the catabolic state of adipocytes, ameliorates metabolic flexibility, and insulin sensitivity. Finally, in cohorts of obese/diabetic patients, we describe a p53 polymorphism that links to long-term efficacy of a fasting-mimicking diet and that the expression of LAM markers and p53 in AT negatively correlates with maintaining weight loss after bariatric surgery. Overall, our results demonstrate that p53 signaling in adipocytes dictates LAM accumulation in AT under IF and that adipocyte p53 modulates fasting effectiveness in mice and humans.
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Project description:Intermittent fasting (IF) reduces cardiovascular risk factors in animals and humans, and can protect the heart against ischemic injury in models of myocardial infarction, but the underlying molecular mechanisms are unknown. To delineate molecular perturbations in response to IF, we carried out comprehensive analyses of molecular pathways and biological processes using proteomic and phosphoproteomic data followed by functional analysis of hearts from mice maintained for 6 months on either daily 12- or 16-hour fasting, every-other-day fasting or ad libitum control feeding regimens. IF regimens significantly affected pathways that regulate cyclic GMP signaling, lipid and amino acid metabolism, cell adhesion, cell death and inflammation. Comparison of differentially expressed proteome and transcriptome upon IF showed higher correlation of pathway alternation in early IF regimen, but inverse correlation of metabolic processes such as fatty acid oxidation and immune processes in later IF regimens. Echocardiographic analyses demonstrated that IF enhances stress-induced cardiac performance. In addition to providing a valuable resource, our systemic analyses reveal molecular framework for understanding how IF impacts the function of the heart and its vulnerability to injury and disease.
2023-09-27 | PXD015452 | Pride
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Project description:Intermittent fasting (IF) increases lifespan, decreases metabolic disease phenotypes, and cancer risk in model organisms, but the mechanisms mediating these effects are not fully characterized. In particular, the altered transcriptional programming has yet to be defined in key fasting responsive tissues such as liver from animals undergoing intermittent fasting. In this study, we employed every-other-day-fasting (EODF) in mice and high-resolution proteome analysis of liver and blood plasma as a screening tool to identify key regulated pathways with comparison to ad libitum fed animals. We observed many changes in the liver proteome abundance profile that were distinct from those observed after a single bout of fasting. Key among these were the induction by EODF of de novo lipogenesis (DNL) and cholesterol biosynthesis pathway enzymes, which were mirrored by related metabolite changes such as increased triacylglycerides and HMG-CoA in EODF liver of fed mice. Paradoxically, we also observed the up-regulation of mitochondrial proteins associated with fatty-acid beta oxidation including ACOT2, which is known to accelerate this pathway in vivo. The most surprising observation was the EODF-mediated 16-fold down-regulation of alpha-1-antitrypsin (SERPINA1E) in liver, which is an abundant plasma protein made exclusively in this tissue. Plasma proteome analysis confirmed a 3-fold decrease in SERPINA1E after 2 weeks of EODF among other significant changes such as increased levels of APOA4, a finding in common with previous human EODF intervention studies. We determined that in liver the SREBP1c and HNF4A transcription factors were playing a major role in the up-regulation of lipid/cholesterol synthesis and down-regulation of AAT, respectively. Further characterization of HNF4A function suggested a global inhibition of its ability to bind promoters of target genes in livers from EODF animals, which we hypothesize is mediated by either increased linoleic acid binding, or post translational modifications of HNF4A protein in EODF animal liver tissue. Together these data provide a comprehensive Omics resource highlighting the key changes observed during the intermittent fasting response in a model animal.
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Project description:This study describes the effects of intermittent fasting induced weight loss on metabolic and molecular pathways
2023-07-01 | GSE196335 | GEO
Project description:We reported a 28-day Intermittent fasting (IF) regimen improved cognitive deficits in db/db mice via a microbiota-metabolites-brain axis assessed by behavioral tests and multiple-omics analysis (transciptomics, 16S rRNA sequencing and metabolomics). Here we present transcriptomics data of mice hippocampus. A total of 310.85Gb clean RNA-SEQ reads of all mice with an average depth of 3.86x were obtained and were then mapped against the Mus musculus genome to obtain the gene expression FPKM values for each sample. We detected 27,094 genes (including 1,345 new predicted genes with no annotation) with FPKM value. Among them, 1,181 genes were found to be only highly expressed in db/db-IF mice compared to db/db and db/m mice, using Differentially Expressed Genes (DEG) analysis, most of which enriched in mitochondrial-related GO terms. Besides, IF strongly elevated genes related to KEGG pathway of oxidative phosphorylation (OXPHOS) via up-regulating mitochondrial located genes expression. In consistent with results from RNA-sequencing analysis, the qPCR analysis confirmed that mitochondrial and metabolic genes expressed were upregulated by IF in db/db mice. In conclusion, IF regimen significantly enhanced mitochondrial and energy metabolism related genes expressions in diabetic mice hippocampus.
2020-02-01 | GSE125387 | GEO
Project description:Intermittent fasting (IF) is a dietary regimen aimed to restrict energy intake via alternate periods of ad libitum food consumption and fasting, without compromise of nutritional composition intake. Prophylactic IF have been well-established in many animal studies to promote longevity as well as ameliorate the development and manifestation of age-related diseases such as cardiovascular, neurodegenerative as well as metabolic diseases. However, while vast experimental evidences have pointed out that IF is able to exert plethora effects against these diseases, understanding with regards to the underlying mechanisms remain in their infancy. Recently, an emerging area of research in the field of epigenetics have been shown to be a cornerstone in mediating the interaction between environmental factors and genome status. IF is a lifestyle intervention that may serves as potential environmental influences over the epigenome status of individuals. However, there is no current information available that shows that IF can induce epigenetic changes. Here, we show that IF is able to influence the modulation of histone H3 lysine 9 trimethylation (H3K9me3) epigenetic mark in C57/BL6 male mice cerebellum, which in turn helps to control a plethora of transcriptomic changes involved in robust metabolic switching processes commonly observed during IF. Interestingly, both epigenomic and transcriptomic modulation are still observed following a refeeding regimen, which may suggest the possibility of epigenetic maintenance induced by IF at this epigenetic locus. However, we found a loss of H3K9me3 maintenance of transcriptomic changes after abolishment of IF. Collectively, our study helps to characterize a novel mechanism of IF in the epigenetic-transcriptomic axis, which control a myriad of metabolic process changes that provide better understanding of IF-induced effects.
2019-08-19 | GSE135945 | GEO