Short-term intensive fasting rejuvenates erythropoiesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA827182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18771824.fastq.gz | Fastqsanger.gz | |||
| SRR18771825.fastq.gz | Fastqsanger.gz | |||
| SRR18771826.fastq.gz | Fastqsanger.gz | |||
| SRR18771827.fastq.gz | Fastqsanger.gz | |||
| SRR18771828.fastq.gz | Fastqsanger.gz |
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Project description:How erythropoiesis responds to fasting remains to be explored. Here, Xu et al. showed that short-term intensive fasting promotes the production of red blood cells and boosts their functions by regulating MS4A3-CDK2 module to enhance megakaryocyte-erythroid progenitor self-renewal and erythroid-biased differentiation.
2023-01-02 | GSE200918 | GEO
Project description:Previous studies have shown that long-term light or moderate fasting such as intermittent fasting can improve health and prolong lifespan. However, in humans short-term intensive fasting, a complete water-only fasting has little been studied. Here, we used multi-omics tools to evaluate the impact of short-term intensive fasting on immune function by comparison of the CD45+ leukocytes from the fasting subjects before and after 72-h fasting. Transcriptomic and proteomic profiling of CD45+ leukocytes revealed extensive expression changes, marked by higher gene upregulation than downregulation after fasting. Functional enrichment of differentially expressed genes and proteins exposed several pathways critical to metabolic and immune cell functions. Specifically, short-term intensive fasting enhanced autophagy levels through upregulation of key members involved in the upstream signals and within the autophagy machinery, whereas apoptosis was reduced by down-turning of apoptotic gene expression, thereby increasing the leukocyte viability. When focusing on specific leukocyte populations, peripheral neutrophils are noticeably increased by short-term intensive fasting. Finally, proteomic analysis of leukocytes showed that short-term intensive fasting not only increased neutrophil degranulation, but also increased cytokine secretion. Our results suggest that short-term intensive fasting boost immune function, in particular innate immune function, at least in part by remodeling leukocytes expression profile.
| S-EPMC8590100 | biostudies-literature
Project description:Background and study aims
We would like to find out whether it is possible for people to follow a short-term fast before their chemotherapy. Fasting involves avoiding all food for a set amount of time. Some research suggests that fasting might help to protect our cells during chemotherapy, by switching them from a state of growth and development to a state of maintenance and repair. However, we don’t know if fasting is of benefit. Ultimately, we would like to find out whether fasting before chemotherapy can help to reduce its side effects. In order to answer this question, we first need to find out whether it is possible for people to fast before their chemotherapy. This has been tested in some previous studies but not in people receiving chemotherapy for colorectal cancer. So, we are inviting 30 people to take part in a trial that will compare a 36-hour fast to usual diet before chemotherapy.
Who can participate?
Adults with stage 2 or 3 colorectal cancer who are due to receive capecitabine oxaliplatin (CAPOX) chemotherapy.
What does the study involve?
Participants will be randomly allocated to either the intervention group or the control group.
The intervention group will spend 36 hours prior to their chemotherapy fasting and drinking water-only. Each chemotherapy cycle will be 21 days long and participants in this group will fast before each of their first 3 cycles of chemotherapy.
The control group will receive the usual advice prior to their first cycle of chemotherapy, including written or verbal information on their diet and the effects of chemotherapy on appetite.
| 2412952 | ecrin-mdr-crc
Project description:Purpose: Next-generation sequencing (NGS) of small RNAs allows transcriptome level analysis of the miRNAome. The goals of this study are to identify differentially regulated hepatic miRNAs in response to a short term fast using small RNA next generation sequencing. Specific quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods were used to validate optimal high-throughput data analysis, and in silico prediction to identify bona fide target pathways regulated by differentially regulated miRNAs following this fasting stressor. Method: Small RNA sequencing was performed using four randomly selected samples from each treatment group were used for sequencing. The quality of total RNA was confirmed by RNA Integrity Numbers greater than 9.0 using an Agilent Technologies 2100 Bioanalyzer. Nucleotide fractions (15-50) of small RNA were isolated from the total RNA using polyacrylamide gel electrophoresis and were ligated to a 30 adapter followed by a 50 adapter (Illumina, San Diego, CA, USA). The small RNA ligated to the adaptors was reverse transcribed to cDNA, PCR amplified and gel purified. The gel-extracted cDNA was used for library preparation, which was further used for cluster generation on Illumina's Cluster Station before sequencing using Illumina GAIIx. Raw sequence data was obtained from image data using Illumina's Sequencing Control Studio software version 2.8 (SCS v2.8) following real-time sequencing image analysis and base-calling by Illumina's Real-Time Analysis version 1.8.70 (RTA v1.8.70). The ACGT101-miR v4.2 pipeline (LC Sciences) was used to analyze sequenced data. Sequences with low Q scores, reads mapped to mRNA, RFam, Repbase and piRNA database were deleted and unique families were generated from identical sequences. These filtered unique sequences were then mapped to fish pre-miRNA and miRNA using miRBase or to the rainbow trout genome (Berthelot et al., 2014) to identify conserved miRNA following ACGT-101 User's Manual. Unique or novel miRNAs were identified after the BLAST performed against fish miRNAs from miRbase database (release 21) and published miRNAs from rainbow trout (Mennigen et al., 2016). The miRNAs that do not match any sequences in the specified databases and have the propensity of forming hairpin structure with the extended sequences at the mapped positions were classified as unique miRNAs. These unique miRNAs were further classified into different groups depending on the mappable reads to selected miRNAs in miRbase. Differentially expressed miRNAs were identified using the statistical software R (Version 3.2.2) package DESeq2 for one-way ANOVA comparison of all three treatment groups. Real-time RT–PCR validation was performed using SYBR Green assays Results: 11 miRNA differentially regulated by fasting. 4 miRNAs are downregulated with fasting. 7 miRNAs are upregulated with fasting. Conclusions: Our study represents the first detailed analysis of the rainbow trout miRNAome in response to nutritional stimuli. Specifically, we here identify common hepatic miRNAs differentially regulated by refeeding following a short-term fast (2d), as well as miRNAs differentially regulated in the postprandial state depending on the dieatary stimulus (no carbohydrates compared to >20% dietary carbohydrates)
2021-04-06 | GSE112816 | GEO
Project description:Heart failure with preserved ejection fraction (HFpEF) is characterised by a distinct but poorly understood in skeletal muscle pathology. In a rat model ZSF1, we identify impaired myonuclear accretion as a mechanism for ablated myofiber growth in HFpEF following resistance exercise intervention. Muscle vascular or mitochondrial dysfunction, or impaired protein synthesis signalling, do not appear as primary limiting mechanisms, and cardiac therapies do not attenuate skeletal muscle pathology. However, we identify that acute caloric restriction rejuvenates myofiber growth in HFpEF during resistance exercise intervention.
2025-01-19 | E-MTAB-12494 | biostudies-arrayexpress
Project description:This study will evaluate the ability of short-term fasting to reduce chemotherapy toxicity and enhance anti-tumour response in patients with colorectal carcinoma subjected to chemotherapy.
| 2328410 | ecrin-mdr-crc
Project description:Interventions: 2:fasting;1:control(normal diet);3:shorten fasting
Primary outcome(s): Absolute and relative changes of peripheral blood mononuclear cells (PBMCs);NLR score of perioperative immune function changes
Study Design: Parallel
| 2696423 | ecrin-mdr-crc
Project description:BackgroundFasting is known to influence the immune functions of leukocytes primarily by regulating their mobilization and redistribution between the bone marrow and the peripheral tissues or circulation, in particular via relocalization of leukocytes back in the bone marrow. However, how the immune system responds to the increased risk of invasion by infectious pathogens with fewer leukocytes in the peripheral blood during fasting intervention remains an open question.ResultsWe used proteomic, biochemical and flow cytometric tools to evaluate the impact of short-term intensive fasting (STIF), known as beego, on red blood cells by profiling the cells from the STIF subjects before and after 6 days of fasting and 6 days of gradual refeeding. We found that STIF, by triggering the activation of the complement system via the complement receptor on the membrane of red blood cells, boosts fairly sustainable function of red blood cells in immune responses in close relation to various pathogens, including viruses, bacteria and parasites, particularly with the pronounced capacity to defend against SARS-CoV-2, without compromising their oxygen delivery capacity and viability.ConclusionSTIF fosters the immune function of red blood cells and therefore, it may be considered as a nonmedical intervention option for the stronger capacity of red blood cells to combat infectious diseases.
| S-EPMC10469874 | biostudies-literature
Project description:Short term fasting changes the hepatic miRNAome in rainbow trout, Oncorhynchus mykiss
| PRJNA449078 | ENA
Project description:Disruption of autophagy--a key homeostatic process in which cytosolic components are degraded and recycled through lysosomes--can cause neurodegeneration in tissue culture and in vivo. Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy. One well-recognized way of inducing autophagy is by food restriction, which upregulates autophagy in many organs including the liver; but current dogma holds that the brain escapes this effect, perhaps because it is a metabolically privileged site. Here, we have re-evaluated this tenet using a novel approach that allows us to detect, enumerate and characterize autophagosomes in vivo. We first validate the approach by showing that it allows the identification and characterization of autophagosomes in the livers of food-restricted mice. We use the method to identify constitutive autophagosomes in cortical neurons and Purkinje cells, and we show that short-term fasting leads to a dramatic upregulation in neuronal autophagy. The increased neuronal autophagy is revealed by changes in autophagosome abundance and characteristics, and by diminished neuronal mTOR activity in vivo, demonstrated by a reduction in levels of phosphorylated S6 ribosomal protein in Purkinje cells. The increased abundance of autophagosomes in Purkinje cells was confirmed using transmission electron microscopy. Our data lead us to speculate that sporadic fasting might represent a simple, safe and inexpensive means to promote this potentially therapeutic neuronal response.
| S-EPMC3106288 | biostudies-literature