Transcriptomic changes in Drosophila tissues under Time-restricted Feeding (TRF)
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE64108 | GEO | 2015/02/18
SECONDARY ACCESSION(S): PRJNA270175
REPOSITORIES: GEO
Similar Datasets
Project description:Next generation sequencing was used to assess the changes along a diurnal cycle in the transcriptome of Drosophila head, periphery (entire body except the head) or the heart at 3, 5 or 7 weeks of age under ad libitum feeding (ALF) or time-restricted feeding (TRF). Next generation sequencing was used to assess the changes along a diurnal cycle in the transcriptome of Drosophila head, periphery (entire body except the head) or the heart at 3, 5 or 7 weeks of age under ad libitum feeding (ALF) or time-restricted feeding (TRF).
2015-02-18 | E-GEOD-64108 | biostudies-arrayexpress
Project description:The goal of the study was to investigate the mechanistic basis for Time-restricted feeding (TRF) improvement in skeletal muscle by assessing transcriptomic data of wild type (WT), WT under High-fat diet (HFD), and genetic obesity linked mutant sphingosine kinase 2 (Sk2) under ad libitum feeding (ALF) and time-restricted feeding (TRF) conditions. Next generation sequencing was used to assess the changes along a diurnal cycle in the transcriptome of Drosophila indirect flight muscle (IFM) tissue at 3-week of age under ad libitum feeding (ALF) or time-restricted feeding (TRF).
2023-01-19 | GSE205334 | GEO
Project description:Time-restricted feeding (TRF) is an emerging behavioral nutrition intervention that sustains a daily cycle of feeding and fasting. TRF in animals and humans has shown pleiotropic health benefits arising from multiple organ systems, yet the molecular basis of TRF is not well understood. We subjected mice to isocaloric ad libitum feeding (ALF) or TRF of Western diet, and examined gene expression changes in 22 different brain regions and peripheral organs collected every 2 hour over 24 hour. We discovered TRF profoundly impacts gene expression. Nearly 80% of genes show significant differential expression or rhythmicity under TRF in at least one tissue. Functional annotation of these changes highlight tissue and pathway specific impacts of TRF. These findings and resources will offer a framework for future mechanistic studies, and guide human TRE interventions for various disease conditions with or without pharmacotherapies.
2022-12-20 | GSE190389 | GEO
Project description:Restricted feeding impacts the hepatic circadian clock of WT mice. Cry1, Cry2 double KO mice lack a circadian clock and are thus expected to show rhythmical gene expression in the liver. Imposing a temporally restricted feeding schedule on these mice shows how the hepatic circadian clock and rhythmic food intake regulate rhythmic transcription in parallel Cry1, Cry2 double KO mice were entrained either to ad libitum or temporally restricted feeding (tRF) schedules. Food was made available to mice under the tRF regimen only between ZT(CT)1 and ZT(CT)9. Mice were then released into constant darkness while the respective feeding schedules were still maintained. Liver tissue was collected on the second day of constant darkness at the indicated timepoints. Total RNA was extracted and 5ug of RNA was used in the standard Affymetrix protocol for amplification, labeling and hybridization
2009-11-23 | E-GEOD-13062 | biostudies-arrayexpress
Project description:Objective: The early consumption of calorie-rich diet disrupts circadian rhythms and has adverse effects on memory, yet the effects of timerestricted feeding (TRF) and the underlying molecular mechanisms are unknown. Here, we set out to identify the behavioral and molecular circadian rhythms disruptions generated by juvenile obesogenic diet consumption and their restoration by TRF in male mice. Methods: Metabolic rhythms were measured by indirect calorimetry and memory performances by behavioral tasks. Hippocampal translatome (pS6_TRAP), enrichment and co-regulated gene network analyses were conducted to identify the molecular pathways involved in memory impairments and their restoration by TRF. Differential exon usage analyses, mass spectrometry and pharmacological intervention were used to confirm thyroid hormone signaling involvement. Results: We show that four weeks of TRF restore the rhythmicity of metabolic parameters and prevents memory impairments in mice fed a high fat-high sucrose (HFS) diet since weaning, independently of body fat levels. Hippocampal translatome and differential exon usage analyses indicate that impaired memory of mice under ad libitum HFS diet is accompanied by reduced thyroid hormone signaling and altered expression of astrocytic genes regulating glutamate neurotransmission. TRF restored the diurnal expression variation of part of these genes and intrahippocampal infusion of T3, the active form of thyroid hormone, rescues memory performances and astrocytic gene expression of ad libitum HFS diet-fed mice. Conclusions: Thus, thyroid hormones contribute to the TRF positive effects on both metabolism and memory in mice fed an obesogenic diet, highlighting this nutritional approach as a powerful tool in addressing obesity brain comorbidities and paving the way for further mechanistic studies on hippocampal thyroid signaling.
2024-11-18 | GSE267751 | GEO
Project description:To further character the significant changes in renal gene expression after time restricted feeding (TRF) treatment in CKD mice,RNA-sequencing was performed in the kidneys.
2021-11-24 | GSE189377 | GEO
Project description:The circadian clock and rhythmic food intake are both important regulators of rhythmic gene expression in the liver. It remains, however, elusive to which extent the circadian clock network and natural feeding rhythms contribute to rhythmic gene expression. To systematically address this question, we developed an algorithm to investigate differential rhythmicity between a varying number of conditions. Mouse knockout models of different parts of the circadian clock network (Bmal1, Cry1/2, and Hlf/Dbp/Tef) exposed to controlled feeding regimens (ad libitum, night restricted feeding) were generated and analyzed for their temporal hepatic transcriptome. A genetical ablation of core loop elements altered feeding patterns that were restored by night restricted feeding. Mainly genes with a high amplitude were driven by the circadian clock but natural feeding patterns equally contributed to rhythmic gene expression with lower amplitude. We observed that Bmal1 and Cry1/2 KOs differed in rhythmic gene expression and identified differences in mean expression levels as a predictor for rhythmic gene expression. In Hlf/Dbp/Tef KO, mRNA levels of Hlf/Dbp/Tef target genes were decreased, albeit rhythmicity was overall preserved potentially due to the activity of the D-Box binding repressor NFIL3. Genes that lost rhythmicity in Hlf/Dbp/Tef KOs were identified to be no direct targets of PARbZip factors and presumably lost rhythmicity due to indirect effects. Collectively, our findings provide unprecedent insights into the diurnal transcriptome in mouse liver and defines the contribution of subloops of the circadian clock network and natural feeding cycles. The developed algorithm and a webapp to browse the outcomes of the study are publicly available to serve as a resource for the scientific community.
2020-12-03 | GSE135898 | GEO
Project description:Circadian rhythm disruption (CD) is associated with dysregulation of glucose homeostasis and Type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates CD-induced metabolic dysfunction. Herein we utilized an approach encompassing analysis of behavioral, physiological, transcriptomic, and single-cell epigenomic effects of CD and consequences of restoration of fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β-cell function and loss of circadian β-cell transcriptional and epigenetic control. In contrast, restoration of fasting/feeding cycle prevented CD-mediated metabolic dysfunction by reestablishing circadian regulation of glucose tolerance, β-cell function, β-cell transcriptional profile, and reestablishment of proline and acidic amino acid-rich basic leucine zipper (PAR-bZIP) transcription factor activity in β-cells. This study provides mechanistic insights into beneficial effects of tRF and its role in prevention of β-cell failure in T2DM.
2021-11-24 | GSE182936 | GEO
Project description:Circadian rhythm disruption (CD) is associated with dysregulation of glucose homeostasis and Type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates CD-induced metabolic dysfunction. Herein we utilized an approach encompassing analysis of behavioral, physiological, transcriptomic, and single-cell epigenomic effects of CD and consequences of restoration of fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β-cell function and loss of circadian β-cell transcriptional and epigenetic control. In contrast, restoration of fasting/feeding cycle prevented CD-mediated metabolic dysfunction by reestablishing circadian regulation of glucose tolerance, β-cell function, β-cell transcriptional profile, and reestablishment of proline and acidic amino acid-rich basic leucine zipper (PAR-bZIP) transcription factor activity in β-cells. This study provides mechanistic insights into beneficial effects of tRF and its role in prevention of β-cell failure in T2DM.
2021-11-24 | GSE182933 | GEO
Project description:Circadian rhythm disruption (CD) is associated with dysregulation of glucose homeostasis and Type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates CD-induced metabolic dysfunction. Herein we utilized an approach encompassing analysis of behavioral, physiological, transcriptomic, and single-cell epigenomic effects of CD and consequences of restoration of fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β-cell function and loss of circadian β-cell transcriptional and epigenetic control. In contrast, restoration of fasting/feeding cycle prevented CD-mediated metabolic dysfunction by reestablishing circadian regulation of glucose tolerance, β-cell function, β-cell transcriptional profile, and reestablishment of proline and acidic amino acid-rich basic leucine zipper (PAR-bZIP) transcription factor activity in β-cells. This study provides mechanistic insights into beneficial effects of tRF and its role in prevention of β-cell failure in T2DM.
2021-11-24 | GSE182931 | GEO