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Determine the effects of mTORC1 inhibition by rapamycin on mouse liver transcriptome

ABSTRACT: Liver from RICTOR knockout mice show normal levels of mTORC1 signaling in response to refeeding. With this experiment we sought to compare the effects of Rictor depletion to the effects of mTORC1 inhibition by rapamycin in liver from mice that were fasted and refed.

ORGANISM(S): Mus musculus

PROVIDER: GSE46582 | GEO | 2013/09/23

SECONDARY ACCESSION(S): PRJNA201041

REPOSITORIES: GEO

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Determine the effects of mTORC1 inhibition by rapamycin on mouse liver transcriptome

Project description:Liver from RICTOR knockout mice show normal levels of mTORC1 signaling in response to refeeding. With this experiment we sought to compare the effects of Rictor depletion to the effects of mTORC1 inhibition by rapamycin in liver from mice that were fasted and refed. Mice were either fasted for 24hr (n=5), or fasted for 22hr then treated with either 10mg/kg rapamycin suspended in 0.9% NaCl and 2% ethanol at a concentration of 1mg/ml (547mM), or vehicle only. After an additional 2 hr, one group of mice (0 hr time, n=3) was sacrificed, the liver immediately removed, and flash frozen in liquid nitrogen. The remaining mice were given ad libitum access to food and sacrificed after 3hr (n=3), 6hr (n=3), or 12 hr (n=3). Two other nonfasted groups of mice (n=2) were injected with either vehicle or rapamycin and sacrificed after 24hr. Submitter cannot locate the CEL files.

2013-09-23 | E-GEOD-46582 | biostudies-arrayexpress

Post-fast refeeding enhances intestinal stem cell mediated regeneration and tumorigenesis through mTORC1 signaling and polyamine

Project description:For more than a century, fasting regimens have been shown to improve health, lifespan, and tissue regeneration in diverse model organisms and humans. However, important questions remain regarding how fasting and refeeding cycles stimulate stem cell output and how this influences their role in early tumor formation. Here, we demonstrate that in the mammalian intestine, a short 24-hour fast followed by a 24-hour refeeding period (that is, post-fast refeeding) and not fasting itself elevates the stemness program and regenerative capacity of Lgr5+ intestinal stem cells (ISCs). Furthermore, loss of the tumor suppressor APC in post-fast refed ISCs significantly boosts tumor incidence in the small intestine and colon compared to those in the fasted or ad libitum fed states. Mechanistically, robust induction of insulin-PI3K-mTORC1 signaling as well as elevated intestinal polyamines level increase protein synthesis in post-fast refed ISCs to mediate these changes as inhibition of mTORC1, polyamine, or protein synthesis abrogate the regenerative or tumorigenic effects of post-fast refeeding. Thus, our data indicate that post-fast refeeding leads to a burst not only in stem cell-driven regeneration but also in tumorigenicity and that careful consideration be given to fast-refeeding cycles when planning diet-based strategies.

2023-08-08 | GSE192482 | GEO

Hepatic gene expression profiles during fed–fasted–refed state in mice [miRNA-seq]

Project description:Regulation of nutrient status during fasting and refeeding plays an important role in maintaining metabolic homeostasis in the liver. Thus, we investigated the impact of the physiological fed–fasted–refed cycle on hepatic gene expression in nutrient-sensitive mice. We performed transcriptomic analysis of liver samples in fed, fasted and refed groups of mice. Through mRNA-sequencing (RNA-Seq) and miRNA-Seq, we compared fasted and fed states (fasted versus fed cohort) as well as refed and fasted states (refed versus fasted cohort) to detect dynamic alterations of hepatic mRNA– miRNA expression during the fed–fasted–refed cycle

2023-02-24 | GSE225696 | GEO

Hepatic gene expression profiles during fed–fasted–refed state in mice [mRNA-seq]

2023-02-24 | GSE225695 | GEO

Expression data from mouse model using targeted deletion of hepatic RICTOR (Albumin-Cre Rictor LoxP/LoxP)

Project description:Recent work using mouse models has revealed that mTORC2, which unlike mTORC1 is not acutely sensitive to rapamycin, plays a key role in the regulation of organismal physiology. The substrates and pathways regulated by mTORC2 are at present relatively unknown Using a mouse model with a targeted deletion of hepatic RICTOR, we investigated the loss of mTORC2 on the murine liver transcriptome Rictor floxed (RKO) and control mice (n=4 per group) were fasted overnight, refed for 3 hr, then sacrificed. Livers were removed, rinsed in PBS, and flash frozen in liquid nitrogen. RNA was extracted and hybridized to Affymetrix Genechip Mouse Gene 1.0 ST arrays

2013-09-23 | E-GEOD-46515 | biostudies-arrayexpress

Effects of extensive fasting and subsequent feeding on hepatic transcription

Project description:Temporally restricted feeding has a profound effect on the circadian clock. Fasting and feeding paradigms are known to influence hepatic transcription. This dataset shows the dynamic effects of refeeding mice after a 24hour fasting period. Mice were entrained for two weeks under ad libitum access to food. Mice were then released into constant darkness and food was withdrawn at CT4 on the first day in constant darkness. On the second day in constant darkness mice were either fed (Refed) or continously fasted (Fast) at CT4. Liver tissue was collected at the indicated timepoints. Total RNA was extracted and standard Affymetrix protocol were used for amplification, labeling and hybridization

2009-11-23 | E-GEOD-13063 | biostudies-arrayexpress

Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice fed ad libitum, fasted for 24 hours and re-fed

Project description:If the function of the nuclear receptor PPARa is well-known during a prolongated fasting, its hepatic biological function during feeding and refeeding conditions still needs to be investigated. Moreover, in vivo data collected so far on PPARa function during fasting were obtained using the total Ppara KO transgenic mouse model. To identify genes whose expression is under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice under three nutritional challenges. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice fed ad libitum, fasted for 24 hours and refed. There are 52 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 8 week-old from the same genetic background (C57Bl/6J) fed ad libitum, fasted for 24 hours, fasted for 24 hours and then refed 24 hours more with glucose added in water (200g/l). In fed condition (Fed), n= 3 mice for LKO, LWT genotypes, n= 5 for KO and n= 4 fot WT; in fasting condition (Fas), n=5 for LKO, LWT and WT genotypes and n= 3 for KO; in refeeding condition (Ref), n= 5 for LKO, KO and WT genotypes and n= 4 for LWT. All mice were sacrified at ZT14.

2016-02-20 | E-GEOD-73299 | biostudies-arrayexpress

Truncation of Pik3r1 Causes Severe Insulin Resistance Uncoupled From Obesity and Dyslipidaemia by Increased Energy Expenditure

Project description:Both PIK3R1(Y657X) mutant and wild-type C57Bl/6J mice were maintained on chow until 16 weeks old, at which time they were fasted for 16 hours and then refed chow for 6 hours. The tissues were harvested and snap-frozen at three time points: chow diet before overnight fast (ad libitum chow, ALC), after 16 hour fast (overnight fast, ONF), and after 6 hour refeeding (refed 6 hours, RF6).

2020-06-30 | GSE153431 | GEO

mTORC1 Activation is not sufficient to suppress hepatic PPAR-a signalling or ketogenesis

Project description:we examined if the activation of the anabolic program mediated by the activation of the mTorc1 complex in the fasted state could suppress the robust catabolic programing and enhanced Pparα transcriptional of mice with a liver specific defect in mitochondrial long chain fatty acid oxidation (Cpt2L-/- mice). We found that the activation of mTorc1 in the fasted state was not sufficient to repress Pparα responsive genes or ketogenesis.

2021-06-15 | GSE165701 | GEO

Spatial landscapes of the fed, fasted and refed livers from C57BL/6J mice - spatial transcriptomics

Project description:Spatial heterogeneity and plasticity of the mammalian liver is critical for systemic metabolic homeostasis in response to fluctuating nutritional status. Here, we generated a high-resolution transcriptomic landscape of the livers from mice that were either fed chow (fed), fasted for 18 h (fasted), or fasted for 18 h and then refed for 6 h (refed) using spatial transcriptomics (ST) and quantified changes in gene expression. This work provides a critical foundation for future mechanistic studies of liver metabolic heterogeneity and plasticity, and will help to understand the zonated pathology during liver disease progression.

2023-01-12 | GSE222796 | GEO

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