Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intermittent fasting induces rapid hepatocyte proliferation to maintain the hepatostat

ABSTRACT: Nutrient availability fluctuates in most natural populations, forcing organisms to undergo periods of fasting and re-feeding. It is unknown how dietary change influences liver homeostasis. Here, we show that a switch from ad libitum feeding to intermittent fasting (IF) promotes rapid hepatocyte proliferation. Mechanistically, IF- induced hepatocyte proliferation is driven by the combined action of intestinally produced, systemic endocrine FGF15 and localized WNT signaling. IF proliferation re-establishes a constant liver-to-body-mass ratio during periods of fasting and re-feeding, a process termed the hepatostat. This study provides the first example of dietary influence on adult hepatocyte proliferation, and challenges the widely held view that liver tissue is mostly quiescent unless chemically or mechanically injured.

ORGANISM(S): Mouse Mus Musculus

TISSUE(S): Liver

SUBMITTER: Brian DeFelice

PROVIDER: ST002263 | MetabolomicsWorkbench | Mon Aug 01 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Mouse Hepatic Lipid Droplet Proteome under Fasting and Re-Feeding

Project description:One of the key functions of the mammalian liver is lipid metabolism. During fasting, lipid storage in the liver increases in order to reserve and provide energy for cellular functions. Upon re-feeding, this reserve of lipids is rapidly depleted; this change is visible, as the organelles responsible for lipid storage – lipid droplets (LDs) – drastically decrease in size following re-feeding. Little is known regarding LD proteome, or how it changes during the fasting/re-feeding transition. Our study investigated the hepatic LD proteome and how it changes between fasting and re-feeding conditions. For this purpose, LDs were isolated from 4 month-old C57BL/6 mice after a 24 hour fasting period, or a 24 hour fasting period followed by 6 hours of re-feeding. Proteins isolated from these LDs were subject to SDS-PAGE followed by in-gel trypsinization and LC-MS/MS. We identified a combined total of 941 proteins on hepatic LDs, of which 817 had quantifiable extracted ion chromatograms in at least 2 samples (n=6 total) and were not deemed contaminants. 777 of the 817 proteins were observed in both energetic states, with 33 being uniquely observed in fasted LDs, and 7 being uniquely observed in re-fed LDs.

2018-05-25 | PXD005977 | Pride

Steroidogenic Control of Liver Metabolism Through a Nuclear Receptor-Network

Project description:Coupling metabolic and reproductive pathways is essential for the survival of species. However, the functions of steroidogenic enzymes expressed in metabolic-tissues are largely unknown. Here, we show that in the liver, the classical steroidogenic enzyme, Cyp17a1, forms an essential nexus for glucose and ketone metabolism during feed-fast cycles. Both gain- and loss-of-function approaches are used to show that hepatic Cyp17a1 is induced by fasting, catalyses the production of a hormone-ligand (DHEA) for PPARα, and is ultimately required for maintaining euglycemia and ketogenesis during nutrient deprivation. The feedback-loop that terminates Cyp17a1-PPARα activity, and re-establishes anabolic liver metabolism during re-feeding is mapped to postprandial bile acid-signalling, involving the receptors FXR, SHP and LRH-1. Together, these findings represent a novel paradigm of homeostatic control in which nutritional cues feed-forward on to metabolic pathways by influencing extragonadal steroidogenesis.

2020-01-16 | PXD012876 | Pride

Neurotensin regulates proliferation and stem cell function in the small intestine in a nutrient-dependent manner

Project description:Background & Aims: Intestinal stem cells (ISCs) are sensitive to dietary alterations and nutrient availability. Neurotensin (NT), a gut peptide localized predominantly to the small bowel and released by fat ingestion, stimulates the growth of intestinal mucosa under basal conditions and during periods of nutrient deprivation, suggesting a possible role for NT on ISC function. Methods: Lgr5-EGFP, NT wild type (Nt+/+) and Lgr5-EGFP, NT knockout (Nt-/-) mice were fed ad libitum (AL) or fasted for 48 h. Small intestine crypts were examined by RNAseq analysis. Results: Loss of NT impaired crypt cell proliferation and ISC function in a manner dependent on nutrient status. Under nutrient-rich conditions, NT stimulated the expression of genes that promote cell cycle progression, leading to crypt cell proliferation. Under conditions of nutrient depletion, NT stimulated WNT/β-catenin signaling and promoted an ISC gene signature, leading to enhanced ISC function. NT was required for the induction of WNT/β-catenin signaling and ISC-specific gene expression during nutrient depletion, and loss of NT reduced crypt cell proliferation and impaired ISC function and Lgr5 expression in the intestine during fasting. Conclusion: Collectively, our findings establish an evolutionarily conserved role for NT in ISC maintenance during nutritional stress.

2021-09-29 | GSE182828 | GEO

Monocytes re-enter the bone marrow during fasting and alter the host response to infection

Project description:The aim was to investigate transcriptional differences between circulating Ly6Chi monocytes under feeding and fasting/re-feeding conditions Ly6Chi monocytes were sorted from blood after contious feeding or after a 24h fast follwed by a four hour re-feeding period

2023-03-07 | GSE217597 | GEO

Expression profiles of Hif1a mutant and wild type mouse livers subjected to cycles of fasting and re-feeding

Project description:In order to understand the role of heterodimeric hypoxia-inducible factors (HIF) in non-alcoholic fatty liver disease, we subjected wild type and Hif1-alpha mutant mice to nutritional stress conditions imposed by switching from fasting to re-feeding. Liver samples and subsequently RNA were extracted at each time point and used to comprehensively characterise transcriptional changes using microarray technology. We provide biological replicates for each of the conditions.

2022-12-01 | E-MTAB-7040 | biostudies-arrayexpress

Impact of circadian time, feeding-fasting rhythm and the autonomous clock on chromatin accessibility

Project description:Using an "omics"-based approach, we investigated the interaction between the autonomous liver clock and feeding-fasting rhythm. Transcriptomic analysis and subsequent quantification of exonic and intronic reads revealed that transcriptional mechanisms mediate, at least in part, the integration of feeding signals by the liver clock to drive mRNA oscillations. Therefore, we performed ATAC-seq to probe the state of chromatin accessibility genome-wide. While most open chromatin regions are unchanged across genotype, time and feeding status, transcription factor (TFs) footprints showed altered activity of certain TFs in Liver-RE AL vs NF. For example, CEBPB activity is altered in Liver-RE AL and restored in NF, an observation accompanied by restored CEBPB and BMAL1 common target gene oscillations. Finally, metabolomics analysis illustrated the partial rescue of hepatic metabolism in Liver-RE NF compared to AL (extensive carbohydrate pathway oscillations), and made clear that extra-hepatic clocks contribute significantly to metabolic oscillations in the liver, particularly for pathways involving lipids. Please see the associated reference for full results.

2023-04-05 | GSE154902 | GEO

Impact of circadian time, feeding-fasting rhythm and the autonomous clock on the transcriptome

2022-09-13 | GSE158600 | GEO

RNAseq of liver of CD and HFD fed mice in fed or fasted conditions

Project description:The liver is key for maintaining metabolic homeostasis between feeding and fasting in healthy conditions. However, this is dysregulated during high fat diet feeding. What are the transcriptomic changes required for rapid adaptation of the liver to respond to feeding and fasting and how is this altered in the development of metabolic disease?

2022-09-26 | GSE151750 | GEO

Mus musculus

Project description:anti-NONO RIP seq in liver nuclei after fasting and re-feeding

| PRJNA383792 | ENA

anti-NONO RIP seq in liver nuclei after fasting and re-feeding

Project description:In order to identify the RNAs bound by NONO complexes in different nutritional conditions, we carried out RNA immunoprecipitation followed by sequencing (RIP-seq) of NONO from mouse liver nuclei collected at three different times of the day. Samples were collected after fasting (ZT10), 2h after re-feeding (ZT14) and towards the end of the feeding period (ZT22). The co-immunoprecipitated RNA (along with input RNA and unspecific IgG bound RNA) was sequenced.

2018-01-18 | GSE98040 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data