Transcriptional and metabolic changes following repeated fasting and refeeding of adipose stem cells highlight adipose tissue resilience
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1176478 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31090153_1.fastq.gz | Fastqsanger.gz | |||
| SRR31090153_2.fastq.gz | Fastqsanger.gz | |||
| SRR31090154_1.fastq.gz | Fastqsanger.gz | |||
| SRR31090154_2.fastq.gz | Fastqsanger.gz | |||
| SRR31090155_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 66 |
Similar Datasets
Project description:Background: Obesity and related metabolic disorders have reached epidemic levels, calling for diverse therapeutic strategies. Altering nutrient intake, timing and quantity by intermittent fasting seem to elicit beneficial health effects by modulating endocrine and cell signaling net-works. This study explores the impact of cyclic nutrient availability in the form of every-other-day fasting (EODF) on human adipose stem cells (ASCs). Methods: We subjected ASCs to repeated fasting/refeeding (F/R) cycles, mimicking low glucose/high fatty acid (LGHF) conditions, and assessed phenotypic and transcriptomic changes, lipid storage capacity, insulin sensitivity and differentiation potential. Results: Four consecutive F/R cycles induced significant changes in ad-ipogenic gene expression, with upregulation of FABP4 and PLIN1 during fasting, and increased lipid storage in the ASCs. Upon differentiation, ASCs exposed to LGHF conditions retained a transient increase in lipid droplet size and altered fatty acid metabolism gene expression until day 9. However, these changes dissipated by day 15 of differentiation, suggesting a limited duration of fasting-induced transcriptional and adipogenic memory. Despite initial effects, ASCs showed re-silience, returning to a physiological trajectory during differentiation, with respect to gene ex-pression and lipid metabolism. Conclusions: These findings suggest that the long-term effects of EODF on the ASC niche may be transient; emphasizing the ability of the adipose tissue to adapt and restore homeostasis.
2024-12-06 | GSE280110 | GEO
Project description:Fasting-refeeding paradigms result in drastic shifts in metabolism and gene expression patterns. The effect of fasting-refeeding changes between young and old individuals. We sought to decipher the changes in response to fasting-refeeding in young and old animals by profiling gene expression in adipose tissue of killifish Nothobranchius furzeri.
2025-05-10 | GSE296348 | GEO
Project description:Gene expression profile was investigated using zebrafish muscle unger fasting-refeeding conditions. This study revealed fasting-refeeding responsive genes in zebrafish muscle.
2022-05-27 | GSE201273 | GEO
Project description:Lipoprotein lipase (LPL) is responsible for the intravascular catabolism of triglyceride-rich lipoproteins and plays a central role in whole-body energy balance and lipid homeostasis. As such, LPL is subject to tissue-specific regulation in different physiological conditions, but the mechanisms of this regulation remain incompletely characterized. Previous work revealed that LPL comprises a set of proteoforms with different isoelectric points, but their regulation and functional significance have not been studied thus far. Here we studied the distribution of LPL proteoforms in different rat tissues and their regulation under physiological conditions. First, analysis by two-dimensional electrophoresis and Western blot showed different patterns of LPL proteoforms (i.e., different pI or relative abundance of LPL proteoforms) in different rat tissues under basal conditions, which could be related to the tissue-specific regulation of the enzyme. Next, the comparison of LPL proteoforms from heart and brown adipose tissue between adults and 15-day-old rat pups, two conditions with minimal regulation of LPL in these tissues, yielded virtually the same tissue-specific patterns of LPL proteoforms. In contrast, the pronounced down-regulation of LPL activity observed in white adipose tissue during fasting is accompanied by a prominent reconfiguration of the LPL proteoform pattern. Furthermore, refeeding reverts this down-regulation of LPL activity and restores the pattern of LPL proteoforms in this tissue. Importantly, this reversible proteoform-specific regulation during fasting and refeeding indicates that LPL proteoforms are functionally diverse. Further investigation of potential differences in the functional properties of LPL proteoforms showed that all proteoforms exhibit lipolytic activity and have similar heparin-binding affinity, although other functional aspects remain to be investigated. Overall, this study demonstrates the ubiquity, differential distribution and specific regulation of LPL proteoforms in rat tissues and underscores the need to consider the existence of LPL proteoforms for a complete understanding of LPL regulation under physiological conditions.
2024-01-26 | PXD043704 | Pride
Project description:Effect of fasting-refeeding on gene expression in young and old killifsh adipose tissue.
| PRJNA1258963 | ENA
Project description:Human hepatic gene regulations by fasting and refeeding in a mouse model with humanized liver generated from a single donor were reported.
2021-01-06 | GSE130525 | GEO
Project description:Skeletal muscle in fish presents a high plasticity controlled by a dynamic balance between anabolic and catabolic signaling pathways. Decreased food availability can inhibit muscle growth and trigger muscle catabolism pathways, thu promoting muscle atrophy. In contrast, anabolism may be favored during restoration of food supply, promoting the muscle growth. Considering this, we analyzed fast-twitch muscle of juvenile Piaractus mesopotamicus (pacu) submitted to a prolonged fasting (30 days) and refeeding (up to 30 days) using shotgun proteomics and gene expression analysis. The relative rate of weight and length increase, as well as the expression of mafbx and igf -1 genes, suggest that prolonged fasting caused muscle atrophy and that 30 days of refeeding led to partial compensatory growth. Shotgun proteomics analysis identified 99 proteins after fasting and 71 proteins after refeeding periods, of which 23 and 17 were differentially expressed after fasting and after 30 days of refeeding, respectively. Most of these differentially expressed proteins were related to cytoskeleton, muscle contraction and muscle metabolism. Among these, parvalbumin (PVALB), a calcium-binding protein and food allergen, was selected for further RT-qPCR analysis, which showed that pvalb mRNA was not changed after 30 days of fasting and 30 days of refeeding, but it was downregulated after 6h and 24h of refeeding. This suggests a post-transcriptional regulation of PVALB in fish muscle. In conclusion, our results suggest that muscle atrophy and partial compensatory growth caused by prolonged fasting and refeeding affected the muscle proteome and PVALB expression. Our results can contribute to the understanding of muscle anabolic and catabolic pathways in response to changes in food availability.
2019-11-28 | PXD014232 | Pride
Project description:Abhd15 is mainly expressed in adipose tissues and highly upregulated upon adipogenesis. Abhd15 expression is correlated with insulin resistance in obese humans, however its physiological function remains unknown. We used the microarray technology to gain insight into ABHD15’s physiological function by identifying dysregulated genes in BAT from Abhd15-ko mice in comparison to WT mice. We used microarrays to detail the global programme of gene expression in BAT and identified distinct dysregulated genes in response to refeeding
2020-04-28 | GSE98494 | GEO
Project description:The discovery of FoxO1 as an effector of insulin action on gene expression filled a gap in our knowledge of insulin signaling. The metabolic impact of hepatic FoxO1 has been demonstrated in genetic mouse models showing that FoxO1 inhibition can reverse diabetes. However, the gamut of FoxO1 targets is unknown, due to the lack of robust genome-wide chromatin occupancy data. To elucidate the genomic architecture of the FoxO1 effect on liver metabolism, we integrated genome-wide ChIP-seq and RNA-seq. During the physiological transition from fasting to refeeding, hepatic FoxO1 translocated from the nucleus to the cytoplasm. At the same time points, cistrome analysis demonstrated that 60% of FoxO1 target sites were cleared by refeeding. RNA-seq from mice following acute liver-specific FoxO1 ablation allowed us to integrate the data in a comprehensive FoxO1 regulome. We identified four distinct classes of FoxO1 targets. Class I targets are enriched in genes regulating cell homeostasis, have FoxO1 sites clustered in promoters and do not show regulation with fasting/refeeding. Class II is comprised of canonical FoxO1 metabolic targets coordinately regulated with other fasting-inducible TFs, such as PPARA, CREB, and GR through promoters. Class III is enriched in glucose metabolic genes regulated through active enhancers, as detected by H3K4me1 and H3K27ac histone marks. Class IV is comprised of triglyceride (TG) and lipoprotein metabolism genes, regulated through intron sites, and characterized by an uneven response to fasting/refeeding regulation.
2022-05-24 | GSE151545 | GEO
Project description:The discovery of FoxO1 as an effector of insulin action on gene expression filled a gap in our knowledge of insulin signaling. The metabolic impact of hepatic FoxO1 has been demonstrated in genetic mouse models showing that FoxO1 inhibition can reverse diabetes. However, the gamut of FoxO1 targets is unknown, due to the lack of robust genome-wide chromatin occupancy data. To elucidate the genomic architecture of the FoxO1 effect on liver metabolism, we integrated genome-wide ChIP-seq and RNA-seq. During the physiological transition from fasting to refeeding, hepatic FoxO1 translocated from the nucleus to the cytoplasm. At the same time points, cistrome analysis demonstrated that 60% of FoxO1 target sites were cleared by refeeding. RNA-seq from mice following acute liver-specific FoxO1 ablation allowed us to integrate the data in a comprehensive FoxO1 regulome. We identified four distinct classes of FoxO1 targets. Class I targets are enriched in genes regulating cell homeostasis, have FoxO1 sites clustered in promoters and do not show regulation with fasting/refeeding. Class II is comprised of canonical FoxO1 metabolic targets coordinately regulated with other fasting-inducible TFs, such as PPARA, CREB, and GR through promoters. Class III is enriched in glucose metabolic genes regulated through active enhancers, as detected by H3K4me1 and H3K27ac histone marks. Class IV is comprised of triglyceride (TG) and lipoprotein metabolism genes, regulated through intron sites, and characterized by an uneven response to fasting/refeeding regulation.
2022-05-24 | GSE151544 | GEO