Circadian Rhythm Microbiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB48232 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR7132870_1.fastq.gz | Fastqsanger.gz | |||
| ERR7132870_2.fastq.gz | Fastqsanger.gz | |||
| ERR7132880_1.fastq.gz | Fastqsanger.gz | |||
| ERR7132880_2.fastq.gz | Fastqsanger.gz | |||
| ERR7132890_1.fastq.gz | Fastqsanger.gz |
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Project description:The increasing prevalence of obesity and related metabolic disorders represents a growing public health concern. Despite advances in other areas of medicine, a safe and effective drug treatment for obesity has been elusive. Obesity has repeatedly been linked to reorganization of the gut microbiome 1-4 , yet to this point obesity therapeutics have been targeted exclusively toward the human host. Here we show that gut microbe-targeted inhibition of the metaorganismal trimethylamine N-oxide (TMAO) pathway protects mice against the metabolic disturbances associated with diet-induced obesity (DIO) or leptin deficiency (ob/ob). Selective small molecule inhibition of the gut microbial enzyme choline TMA-lyase (CutC) does not significantly reduce food intake, but instead is associated with beneficial remodeling of the gut microbiome, improvement in glucose tolerance, and enhanced energy expenditure. Leveraging untargeted metabolomics we discovered that CutC inhibition is associated with reorganization of host circadian control of both phosphatidylcholine and energy metabolism. Collectively, this study underscores the close relationship between microbe and host metabolism, and provides evidence that gut microbe-derived trimethylamine (TMA) is a key regulator of the host circadian clock. This work also demonstrates that gut microbe-targeted enzyme inhibitors can have profound effects on host energy metabolism, and have untapped potential as anti-obesity therapeutics.
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Project description:The feeding/fasting cycles controlled by our circadian clock impose great daily metabolic and physiological changes, and yet investigations into the consequences of metabolic deficiencies, either dietary or genetic, have often ignored the time of day or the circadian time of the animals or subjects. In addition, these deficiencies may themselves disrupt our circadian clock, causing secondary metabolic, physiological and behavioural disorders. Dietary methionine/choline deficiency in rodents is a common model for human non-alcoholic steatohepatitis, but methionine and choline are nutrients essential for many other processes beyond fatty acid synthesis in the liver, including biological methylations and 1-carbon metabolism, regulation of translation notably via the mTOR pathway, phospholipid synthesis, polyamine pathway and glutathione synthesis. We have previously shown that circadian rhythms in many organisms are highly sensitive to deficiency or excesses of 1-carbon metabolites. Using a methionine/choline deficient diet in mice, we illustrate the nutrigenomic crosstalk between circadian rhythms and 1-carbon metabolism. We show not only that circadian locomotor activity behaviour is profoundly, rapidly and reversibly affected by methionine/choline deficiency, but also that the effects of methionine/choline deficiency on gene expression and 1-carbon metabolites are dependent on circadian time, illustrating the importance of considering circadian rhythms in metabolic studies. This study also highlights the impact of what we eat, or don't, on our behaviour and biological rhythms.
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Project description:In this study we utilized a genome-wide approach to analyze circadian patterns of gene expression in mouse lung lungs, both in the basal state and in the setting of systemic inflammation caused by endotoxemia. We chose the lung because it represents a primary portal for systemic infection and organ failure in critically ill patients, and because the lung exhibits strong physiological circadian rhythms in health and in diseases such as asthma. The gene expression the data presented here was correlated to histological observations and metabolite measurements derived from the same biological samples, in order to obtain a broad picture of how inflammation impacts circadian rhythms in mouse lung.
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Project description:In this study we utilized a genome-wide approach to analyze circadian patterns of gene expression in mouse lung lungs, both in the basal state and in the setting of systemic inflammation caused by endotoxemia. We chose the lung because it represents a primary portal for systemic infection and organ failure in critically ill patients, and because the lung exhibits strong physiological circadian rhythms in health and in diseases such as asthma. The gene expression the data presented here was correlated to histological observations and metabolite measurements derived from the same biological samples, in order to obtain a broad picture of how inflammation impacts circadian rhythms in mouse lung.
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Project description:Observational, non randomized study aimed at measuring the circadian rhythms in the urinary concentrations of physiological modified nucleosides in 30 patients with metastatic colorectal cancer and in 30 age and sex-matched healthy subjects.
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Project description:In this study we utilized a genome-wide approach to analyze circadian patterns of gene expression in mouse lung lungs, both in the basal state and in the setting of systemic inflammation caused by endotoxemia. We chose the lung because it represents a primary portal for systemic infection and organ failure in critically ill patients, and because the lung exhibits strong physiological circadian rhythms in health and in diseases such as asthma. The gene expression the data presented here was correlated to histological observations and metabolite measurements derived from the same biological samples, in order to obtain a broad picture of how inflammation impacts circadian rhythms in mouse lung. To examine circadian regulation in mouse lung we performed 2 independent time-series experiments (Microarray Experiments #1 and #2), in which groups of mice were euthanized at 4 hour intervals for 48 hours. The purpose of Microarray Experiment #1 was to control for environmental influences (light and nutrition) on the detection of circadian rhythms in gene expression. In Microarray Experiment #1, 72 mice were segregated equally into 2 equal groups the day prior to the experiment at the beginning of the dark phase (Circadian Time 12 (CT12) or 7:00 PM local time). In one group (samples labeled with the suffix “MR”) the mice were kept under standard lighting and nutritional conditions (LD 12:12). In the second group (samples labeled with the suffix “DD”), mice were kept in constant darkness and food pellets were removed from their cages at the start of sample acquisition (DD 12:12+STV). Sample acquisition commenced at CT4 (or 11:00 AM local time). For each group 3 animals were sacrificed per time point (12 time points total). For mRNA isolation lung tissue was immersed in RNAlater (Qiagen) and total RNA was then extracted using the RNeasy Mini Kit (Qiagen). RNA quality (RIN>=7) was confirmed using an Agilent 2100 Bioanalyzer. RNA from all biological samples was labeled at once using the Ambion TotalPrep-96 RNA Amplification Kit. The samples were then blinded, randomized to chip position and hybridized to the Illumina MouseRef-8 v2.0 Expression BeadChips. For Microarray Experiment #1 RNA labeling and microarray hybridization were conducted at the Partners Center for Personalized Genetic Medicine. All biological samples were represented by a single technical replicate on the microarray.
2014-07-16 | E-GEOD-59396 | biostudies-arrayexpress
Project description:Circadian rhythms are daily physiological and behavioral changes governed by an internal molecular clock, and dysfunctions in circadian rhythms have long been associated with various neurodegenerative diseases. Abnormal sleep-wake cycle often precedes the onset of cognitive and motor symptoms in patients, while the pathological changes may further exacerbate the disturbance in circadian cycle. It is unclear whether dysregulated circadian rhythm is a consequence of, or a contributing factor for, neurodegeneration. In addition, the evidence directly connecting the neurodegeneration-associated proteins to core circadian clock gene expression remains sparse. Here we show that FUS, a RNA-binding protein implicated in the pathogenesis of ALS and frontotemporal dementia, exhibits a bi-directional regulation with circadian rhythm. Our meta-analysis of RNAseq datasets and subsequent biochemical analysis revealed FUS as a gene regulated by circadian oscillation. Furthermore, NR1D1 binds the FUS promoter and regulates the amplitude of FUS oscillation. Meanwhile, FUS is recruited by transcriptional co-repressor PSF, and is found in the same complex as Bmal-Clock to repress Per2 expression. More strikingly, in cells and brain tissues from homozygous knock-in rats, the pathogenic R521C mutant FUS significantly alters the oscillation patterns of core circadian genes even at young age. Therefore, our results have revealed a novel bi-directional mechanism whereby dysregulated circadian clock and FUS expression may exacerbate neurodegeneration via mutual influence.
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Project description:The circadian clock in murine articular cartilage is a critical temporal regulatory mechanism for tissue homeostasis and osteoarthritis. However, translation of these findings into humans has been hampered by the difficulty in obtaining circadian time series human cartilage tissues. As such, a suitable model is needed to understand the initiation and regulation of circadian rhythms in human cartilage. We used a chondrogenic differentiation protocol on human embryonic stem cells (hESCs) as a proxy for early human chondrocyte development. Chondrogenesis was validated using histology and expression of pluripotency and differentiation markers. The molecular circadian clock was tracked in real time by lentiviral transduction of human clock gene luciferase reporters. Differentiation-coupled gene expression was assessed by RNAseq and differential expression analysis.
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Project description:In this study we utilized a genome-wide approach to analyze circadian patterns of gene expression in mouse lung lungs, both in the basal state and in the setting of systemic inflammation caused by endotoxemia. We chose the lung because it represents a primary portal for systemic infection and organ failure in critically ill patients, and because the lung exhibits strong physiological circadian rhythms in health and in diseases such as asthma. The gene expression the data presented here was correlated to histological observations and metabolite measurements derived from the same biological samples, in order to obtain a broad picture of how inflammation impacts circadian rhythms in mouse lung. To examine circadian regulation in mouse lung we performed 2 independent time-series experiments (Microarray Experiments #1 and #2), in which groups of mice were euthanized at 4 hour intervals for 48 hours. The purpose of Microarray Experiment #2 was to compare circadian gene expression in healthy lungs (samples labeled with the prefix “NT”) to lungs derived from endotoxemic animals (samples labeled with the prefix “LT”). For Microarray Experiment #2, 94 mice were placed under constant light conditions (LL 12:12, food ad libitum) at CT12 the prior day (7:00 PM local time). At CT10 (5:00 PM) on the day of the experiment a sub-group of 40 mice received a single intraperitoneal injection of 12 mg/kg E. coli O127:B8 endotoxin (LPS, Sigma L3129, Lot 029K4055), and sample collection began directly after. 3-4 mice per group were sacrificed at consecutive 4 hour intervals for 2-3 days. The left lung and the right upper lobe were frozen immediately in liquid nitrogen for microarray analysis. For mRNA isolation lung tissue was immersed in RNAlater (Qiagen) and total RNA was then extracted using the RNeasy Mini Kit (Qiagen). RNA quality (RIN>=7) was confirmed using an Agilent 2100 Bioanalyzer. RNA from all biological samples was labeled at once using the Ambion TotalPrep-96 RNA Amplification Kit. The samples were then blinded, randomized to chip position and hybridized to the Illumina MouseRef-8 v2.0 Expression BeadChips. For Microarray Experiment #2 at the Channing Division of Network Medicine (Brigham and Women’s Hospital). Two biological samples (NT00L1 and LT00L1) were represented by 2 technical replicates on the microarray. The remaining biological samples were represented by a single technical replicate.
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