Circadian alignment of early onset caloric restriction promotes longevity in male C57BL/6J mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA788968 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17260300.fastq.gz | Fastqsanger.gz | |||
| SRR17260400.fastq.gz | Fastqsanger.gz | |||
| SRR17260500.fastq.gz | Fastqsanger.gz | |||
| SRR17260301.fastq.gz | Fastqsanger.gz | |||
| SRR17260401.fastq.gz | Fastqsanger.gz |
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Project description:Caloric restriction (CR) prolongs lifespan, yet the mechanisms by which it does so remain poorly understood. Under CR, mice self-impose chronic cycles of 2-hour-feeding and 22-hour-fasting, raising the question whether calories, fasting, or time of day are causal. We show that 30%-CR is sufficient to extend lifespan 10%; however, a daily fasting interval and circadian-alignment of feeding act together to extend lifespan 35% in male C57BL/6J mice. These circadian effects of CR are independent of fasting duration and body weight. Aging induces widespread increases in gene expression associated with inflammation and decreases in expression of genes encoding components of metabolic pathways in liver from ad lib fed mice. CR at night ameliorates these aging-related changes. Thus, circadian interventions promote longevity and provide a perspective to further explore mechanisms of aging.
2022-05-06 | GSE190939 | GEO
Project description:Caloric restriction (CR) prolongs life span, yet the mechanisms by which it does so remain poorly understood. Under CR, mice self-impose chronic cycles of 2-hour feeding and 22-hour fasting, raising the question of if it is calories, fasting, or time of day that is the cause of this increased life span. We show here that 30% CR was sufficient to extend the life span by 10%; however, a daily fasting interval and circadian alignment of feeding acted together to extend life span by 35% in male C57BL/6J mice. These effects were independent of body weight. Aging induced widespread increases in gene expression associated with inflammation and decreases in the expression of genes encoding components of metabolic pathways in liver from ad libitum-fed mice. CR at night ameliorated these aging-related changes. Our results show that circadian interventions promote longevity and provide a perspective to further explore mechanisms of aging.
| S-EPMC9262309 | biostudies-literature
Project description:Caloric restriction (CR) is the only non-genetic intervention to retard aging and increase longevity in a variety of species. It is important to understand the fundamental mechanism by which CR extends lifespan that remains elusive. Owing to well-established genomic tools and convenience of culture system, we used a single cell organism, Saccharomyces cerevisiae, to clarify the mechanisms of CR. In order to identify genes responsible for CR-mediated longevity, we performed microarray experiments across the longevity assurance time-points. Since the CR-treated cells obtained the longevity potential around 12 hours after inoculation and the strength of potential gradually increased up to 48 hours, we concluded that the changes across these time-points must be a critical need for assurance of longevity by CR. For preparation of total RNA, yeast cells under control (2% glucose) and CR (0.5% glucose) conditions were harvested at 12h, 18h, 24h and 48h after inoculation. After total RNA extraction, we performed Affymetrix Yeast GeneChip 2.0 array for biological triplicate repeats according to the manufacturer's instructions.
2013-12-31 | E-GEOD-41860 | biostudies-arrayexpress
Project description:Caloric restriction (CR) is the only non-genetic intervention to retard aging and increase longevity in a variety of species. It is important to understand the fundamental mechanism by which CR extends lifespan that remains elusive. Owing to well-established genomic tools and convenience of culture system, we used a single cell organism, Saccharomyces cerevisiae, to clarify the mechanisms of CR. In order to identify genes responsible for CR-mediated longevity, we performed microarray experiments across the longevity assurance time-points.
2013-12-31 | GSE41860 | GEO
Project description:Transcriptome analysis using the liver from young versus old mice, fed either normally or under caloric restriction reveals reorganization of distinct circadian signatures related to metabolic aging and nutrient-dependent counterbalance of aging by caloric restriction
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Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.
2011-04-29 | E-GEOD-16790 | biostudies-arrayexpress
Project description:Characterization of the fecal metaproteome in rats fed ad libitum or following a caloric restriction diet
2018-10-08 | PXD007252 | Pride
Project description:This study explored the role of the growth hormone (GH) / insulin-like growth factor 1 (IGF-1) axis on the life-long caloric restriction (CR)-associated remodeling of white adipose tissue (WAT). Adipocyte size and gene expression profiles, using high-density oligonucleotide microarrays, were analyzed in WAT of six- to seven-month old wild Wistar rats fed ad libitum (AL) or subjected to a 30% caloric restriction (CR), and heterozygous transgenic dwarf rats bearing an anti-sense GH transgene fed ad libitum (Tg). While not significant in Tg rats, adipocyte size was significantly reduced in CR rats compared with AL rats. The microarray data based on the principal component analysis demonstrated that the gene expression profile of CR rats markedly differed from the AL rats, while Tg hardly differed, suggesting that CR-associated WAT remodeling was predominantly regulated in a GH/IGF-1-independent manner. The gene cluster with the largest change induced by CR included several genes involved in lipid biosynthesis and inflammation. Moreover, many of the genes transcriptionally regulated by sterol regulatory element binding proteins (SREBPs) were found in the cluster related to lipid biosynthesis. Real-time reverse transcription polymerase chain reaction analysis confirmed that the expression of SREBP-1 and its down-stream targets was particularly up-regulated in CR rats compared with SREBP-2 and its down-stream targets. Our findings suggest that SREBP-1 is a major transcription factor in CR-associated remodeling of WAT, and might be one of the key regulators of the anti-aging and pro-longevity effects of CR. The three groups: GH antisense, caloric restriction, and the control were compared by using PCA.
2012-09-27 | E-GEOD-30668 | biostudies-arrayexpress
Project description:Tissue specificity is a fundamental property of an organ that affects numerous biological processes, including aging and longevity, and is regulated by the circadian clock. However, the distinction between circadian-affected tissue specificity and other tissue specificities remains poorly understood. Here, using multi-omics data on circadian rhythms in mice, we discovered that approximately 35% of tissue-specific genes are directly affected by circadian regulation. These circadian-affected tissue-specific genes have higher expression levels and are associated with metabolism and hepatocyte cells. They also exhibit specific features in long-reads sequencing data. Notably, these genes are associated with aging and longevity at both the gene level and at the network module level. The expression of these genes oscillates in response to caloric and time-restricted feeding regimens, which have been demonstrated to promote longevity. In addition, aging and longevity genes are disrupted in various circadian disorders. Our study indicates that the modulation of circadian-affected tissue specificity is essential for understanding the circadian mechanisms that regulate aging and longevity at the genomic level.
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