Transcriptomic signature of fasting in murine adipose tissue
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PROVIDER: PRJNA646777 | ENA |
REPOSITORIES: ENA
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Project description:Little is known about the impact of fasting on gene regulation in human adipose tissue. Accordingly, the objective of this study was to investigate the effects of fasting on adipose tissue gene expression in humans. To that end, subcutaneous adipose tissue biopsies were collected from volunteers 2h and 26h after consumption of a standardized meal. For comparison, epididymal adipose tissue was collected from C57Bl/6J mice after a 16h fast and in the ab-libitum fed state. Transcriptome analysis was carried out using Affymetrix microarrays. We found that, 1) fasting downregulated numerous metabolic pathways in human adipose tissue, including triglyceride and fatty acid synthesis, glycolysis and glycogen synthesis, TCA cycle, oxidative phosphorylation, mitochondrial translation, and insulin signaling; 2) fasting downregulated genes involved in proteasomal degradation in human adipose tissue; 3) fasting had much less pronounced effects on the adipose tissue transcriptome in humans than mi ce; 4) although major overlap in fasting-induced gene regulation was observed between human and mouse adipose tissue, many genes were differentially regulated in the two species, including genes involved in insulin signaling (PRKAG2, PFKFB3), PPAR signaling (PPARG, ACSL1, HMGCS2, SLC22A5, ACOT1), glycogen metabolism (PCK1, PYGB), and lipid droplets (PLIN1, PNPLA2, CIDEA, CIDEC). In conclusion, although numerous genes and pathways are regulated similarly by fasting in human and mouse adipose tissue, many genes show very distinct responses to fasting in humans and mice. Our data provide a useful resource to study adipose tissue function during fasting.
2020-09-01 | GSE154611 | GEO
Project description:Transcriptomic signature of fasting in adipose tissue
| PRJNA646774 | ENA
Project description:Transcriptomic signature of fasting in human adipose tissue
| PRJNA646776 | ENA
Project description:Little is known about the impact of fasting on gene regulation in human adipose tissue. Accordingly, the objective of this study was to investigate the effects of fasting on adipose tissue gene expression in humans. To that end, subcutaneous adipose tissue biopsies were collected from volunteers 2h and 26h after consumption of a standardized meal. For comparison, epididymal adipose tissue was collected from C57Bl/6J mice after a 16h fast and in the ab-libitum fed state. Transcriptome analysis was carried out using Affymetrix microarrays. We found that, 1) fasting downregulated numerous metabolic pathways in human adipose tissue, including triglyceride and fatty acid synthesis, glycolysis and glycogen synthesis, TCA cycle, oxidative phosphorylation, mitochondrial translation, and insulin signaling; 2) fasting downregulated genes involved in proteasomal degradation in human adipose tissue; 3) fasting had much less pronounced effects on the adipose tissue transcriptome in humans than mi ce; 4) although major overlap in fasting-induced gene regulation was observed between human and mouse adipose tissue, many genes were differentially regulated in the two species, including genes involved in insulin signaling (PRKAG2, PFKFB3), PPAR signaling (PPARG, ACSL1, HMGCS2, SLC22A5, ACOT1), glycogen metabolism (PCK1, PYGB), and lipid droplets (PLIN1, PNPLA2, CIDEA, CIDEC). In conclusion, although numerous genes and pathways are regulated similarly by fasting in human and mouse adipose tissue, many genes show very distinct responses to fasting in humans and mice. Our data provide a useful resource to study adipose tissue function during fasting.
2020-09-01 | GSE154610 | GEO
Project description:Prolonged fasting-induced changes in rat white adipose tissue (epidydimal) transcriptome White adipose tissue is a central place to energy storage and a major endocrine organ. However, adipose molecular mechanisms have been poorly studied during prolonged fasting. To fill this gap, the aim of this study was to decipher transcriptomic regulations in rat adipose tissue during phase 2 (lipid mobilization) and phase 3 (protein catabolism) of prolonged fasting compared to the fed state. We describe a regulatory transcriptional program in epididymal adipose tissue in line with lipogenesis repression during both phases, and that would favor lipolysis during phase 2 and repress it during phase 3. Such regulations notably involve selective (i.e. phase-dependent) changes in gene expression levels of lipases, lipid droplet-associated factors, and the proteins involved in cAMP-dependent and cAMP-independent regulation of lipolysis. The mRNA levels of adipose-secreted factors were globally consistent with the repression of insulin signalling during prolonged fasting. Regulations of leptin and adiponectin levels could be related to their respective role in triggering refeeding during late fasting and controlling lipid metabolism. Specific responses reflecting adipose tissue inflammation, increased fibrinolysis and a possible protein catabolism-related energy saving mechanism were also recorded during phase 3. These data thus provide a comprehensive molecular basis of adipose tissue responses according to the fasting stage.
2021-08-23 | GSE118978 | GEO
Project description:The purpose of this experiment was to determine the murine white adipose expression traits that were changed in response to treatment with Rosiglitazone. Keywords: drug treatment response signature
2007-02-17 | GSE7027 | GEO
Project description:The purpose of this experiment was to determine the murine white adipose expression traits that were changed in response to over expressing Zfp90. Keywords: single gene perturbation signature
2007-02-17 | GSE7029 | GEO
Project description:The purpose of this experiment was to determine the murine white adipose expression traits that were changed in response to knocking Alox5 out. Keywords: gene specific knockout signature
2007-02-17 | GSE7026 | 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.
2024-01-16 | PXD041351 | Pride
Project description:Fasting is the process of metabolic adaption to food deprivation that is taking place in most organisms, e.g. during the daily resting phase in mammals. Furthermore, in biomedical research fasting is used in most metabolic studies to synchronize nutritional states of study subjects. Because there is a lack of standardization for this procedure, we need a deeper understanding of the dynamics and the molecular players in fasting. In this study we investigated the transcriptome signature of white adipose tissue, liver, and skeletal muscle in 24 hours fasted mice (and chow fat controls) using Affymetrix whole-genome microarrays. Food was withdrawn from the fasting group at the beginning of the light phase (9 a.m.) when mice are in their inactive phase. Mice were sacrificed 24 hours later by cervical dislocation. Chow-fed controls had ad libitium access to food during this time. Edidymal white adipose tissue, liver, and skeletal muscle were dissected out, shock frozen in liquid nitrogen and stored at -80°C.
2013-11-04 | E-GEOD-46495 | biostudies-arrayexpress