E-MTAB-7040
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ABSTRACT:
PROVIDER: E-MTAB-7040 | ExpressionAtlas | 2023-06-15
REPOSITORIES: ExpressionAtlas
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Project description:Rdh1 is one of the several enzymes that catalyze the first of the two reactions to convert retinol into all-trans-retinoic acid (atRA). Here we show that Rdh1-null mice fed low-fat diet gain more weight as adiposity thann wild-type mice by 20 weeks old, despite neither consuming more calories nor decreasing activity. RNAseq revealed dysregulation of 424 BAT genes in null mice, with segregated predominantly into differences after fasting vs after re-feeding. Rdh1-generated atRA in BAT regulates multiple genes that promote BAT adaptation to whole-body energy status, such as fasting and re-feeding.
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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
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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.
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Project description:The gene expression profiles of WT and NML-KO livers
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Project description:Purpose: To gain a comprehensive understanding of differential gene expression in anadromous C. nasus during feeding and fasting conditions. Methods: we characterized transcriptomics of C. nasus livers between feeding and fasting using RNA-seq Results:A total of 23,159 mRNA moleculeswere selected to identify the mechanisms of feeding and fasting. Our results provide insight into the activation of protein synthesis and energy metabolism, identification of key genes involved in food intake regulation, motivation of the fatty acid biosynthesis, glycolysis, TCA cycle and oxidative phosphorylation and decrease of amino acids and linoleic acid metabolism in feeding conditions compared to fasting. Conclusions:This is the first study describing differential gene expression and metabolic changes accompanying feeding and fasting in this interesting but endangered group. Our findings will be useful for future research on feeding characteristics, energy utilization and survival strategies of C. nasus.
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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.
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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.
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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.
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