Stable isotope resolved analysis of HUVEC Cells under normaxia and hypoxia
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Agilent 5975T LTM GC/MSD (Agilent)
SUBMITTER: Philippe Rocca-Serra
PROVIDER: MTBLS412 | MetaboLights | 2017-12-18
REPOSITORIES: MetaboLights
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MTBLS412 | Other | |||
| FILES | Other | |||
| a_MTBLS412_metabolite_profiling_mass_spectrometry.txt | Txt | |||
| i_Investigation.txt | Txt | |||
| m_MTBLS412_metabolite_profiling_mass_spectrometry_v2_maf.tsv | Tabular |
Items per page: 5 1 - 5 of 7 |
Similar Datasets
Project description:Rhodobacter sphaeroides produces hydrogen gas (H2) via its nitrogenase enzyme during photoheterotrophic growth under nitrogen-limited conditions. We find that cells produce different amounts of H2 and show different growth rates, depending on the organic substrate provided (lactate, succinate, glucose, xylose, or glycerol). We used global transcript analyses to determine what genes are involved in the onset of H2 production, and those that lead to different H2 production capacities in cells fed different organic substrates. Growth and real-time H2 production were followed for photoheterotrophically grown Rhodobacter sphaeroides cultures (19 mL test tube cultures) fed one of five different organic substrates (lactate, succinate, glucose, xylose, or glycerol) and provided glutamate as the sole nitrogen source. Cells were harvested for RNA extraction during early post-exponential growth, at points near the maximum H2 production rates of the cultures. Non-H2-producing cells (500 mL cultures) fed succinate and provided NH4+ as nitrogen source were also harvested for RNA extraction as reference samples. At least two samples for every given set of conditions were analyzed.
2011-08-21 | E-GEOD-29811 | biostudies-arrayexpress
Project description:Background: Exercise mimetics is a proposed class of therapeutics that specifically mimics or enhances the therapeutic effects of exercise. Muscle glycogen and lactate extrusion are critical for physical performance. The mechanism by which glycogen and lactate metabolism are manipulated during exercise remains unclear. This study aimed to assess the effect of miR-92b on the upregulation of exercise training-induced physical performance. Methods: Adeno-associated virus (AAV)-mediated skeletal muscle miR-92b overexpression in C57BLKS/J mice, and global knockout of miR-92b mice were used to explore the function of miR-92b in glycogen and lactate metabolism in skeletal muscle. AAV-mediated UGP2 or MCT4 knockdown in WT or miR-92 knockout mice was used to confirm whether miR-92b regulates glycogen and lactate metabolism in skeletal muscle through UGP2 and MCT4. Body weight, muscle weight, grip strength, running time and distance to exhaustion, and muscle histology were assessed. The expression levels of muscle mass-related and functionrelated proteins were analysed by immunoblotting or immunostaining. Results: Global knockout of miR-92b resulted in normal body weight and insulin sensitivity, but higher glycogen content before exercise exhaustion (0.8538 ± 0.0417 vs 1.043 ± 0.040, **P=0.0087), lower lactate levels after exercise exhaustion (4.133 ± 0.2589 vs 3.207 ± 0.2511, *P=0.0279), and better exercise capacity (running distance to exhaustion, 3616 ± 86.71 vs 4231 ± 90.29, ***P=0.0006; running time to exhaustion, 186.8 ± 8.027 vs 220.8 ± 3.156, **P=0.0028), as compared to those observed in the control mice. Mice skeletal muscle overexpressing miR-92b (both miR-92b-3p and miR-92b-5p) displayed lower glycogen content before exercise exhaustion (0.6318 ± 0.0231 vs 0.535 ± 0.0194, **P=0.0094), and higher lactate accumulation after exercise exhaustion (4.5 ± 0.2394 vs 5.467 ± 0.1892, *P=0.01), and poorer exercise capacity (running distance to exhaustion, 4005 ± 81.65 vs 3228 ± 149.8, ***P＜0.0001; running time to exhaustion, 225.5 ± 7.689 vs 163 ± 6.476, **P=0.001). Mechanistic analysis revealed that miR-92b-3p targets UDP-glucose pyrophosphorylase 2 (UGP2) expression to inhibit glycogen synthesis, while miR-92b-5p represses lactate extrusion by directly target monocarboxylate transporter 4 (MCT4). Knockdown of UGP2 and MCT4 reversed the effects observed in the absence of miR-92b in vivo. Conclusions: This study revealed regulatory pathways, including miR-92b-3p/UGP2/glycogen synthesis and miR-92b-5p/MCT4/lactate extrusion, which could be targeted to control exercise capacity.
2023-10-01 | GSE242294 | GEO
Project description:This study aims to establish a comprehensive, genome-scale metabolic model (GSMM) combining different omics data of different regulatory levels of breast cancer cells in order to elucidate the way that these regulatory levels affect or determine each other. Together with transcriptomics, proteomics and metabolomics data obtained, fluxomics data was also to be integrated. In order to get the fluxomics data, MCF cells were incubated with either the medium containing [1,2-13C2]-D-glucose or [U-13C5]-L-glutamine for 8 or 24 hours. A good GSMM should answer any perturbations applied; therefore, different incubation conditions should be applied to generate different metabolic profiles that will help to test if the model of breast cancer works well. To this end, MCF cells were either administered oligomycine, which is an ATP synthase inhibitor, or were deprived of glutamine. Cells were counted before and after each incubation time so as to get the cell proliferation curve. Later, at the corresponding time points, cells and media were frozen to measure the concentrations of glucose, glutamine and lactate (not shown in the file) and the mass isotopomer distributions of glutamate, ribose, lactate, amino acids and TCA cycle intermediates (shown in the file). Finally, all these data was combined in order to estimate the flux rates of various reactions within the central carbon metabolism (not shown in the file). The fluxomics data obtained in this way is to be introduced in the GSMM designed.
2021-01-18 | MTBLS183 | MetaboLights
Project description:Growth of B. breve UCC2003 on ribose leads to the transcriptional induction of the rbsACBDK gene cluster. Generation and phenotypic analysis of an rbsA insertion mutant established that the rbs gene cluster is essential for ribose utilization, and that its transcription is likely regulated by a LacI-type regulator encoded by rbsR, located immediately upstream of rbsA. Gel mobility shift assays using purified RbsRHis indicate that the promoter upstream of rbsABCDK is negatively controlled by RbsRHis binding to an 18-bp inverted repeat and that RbsRHis binding activity is modulated by D-ribose. The rbsK gene of the rbs operon of B. breve UCC2003 was shown to specify a ribokinase (EC 2.7.1.15), which specifically directs its phosphorylating activity towards D-ribose, converting this pentose sugar to ribose-5-phosphate. In order to investigate differences in global gene expression upon growth of B. breve UCC2003 on ribose, or a combination of ribose and glucose, as compared to glucose, DNA microarray experiments were performed. Total RNA was isolated from B. breve UCC2003 cultures grown on ribose, a combination of ribose and glucose, or glucose. All experiments were performed in duplicate. A dye swap was performed in one of the two biological replicates.
2010-05-19 | E-GEOD-17325 | biostudies-arrayexpress
Project description:The study aimed the effects of Sasa quelpaertensis leaf hot water extract (SQH) on anti-fatigue function and the global gene expression pattern in muscle tissue. When rat skeletal muscle cells were cultured in hypoxic condition, the levels of lactate and lactate dehydrogenase (LDH) was increased approximately more than 2-fold, but SQH decreased effectively these levels. Thus, we assessed the exercise and fatigue recovery function using several physical biomarkers such as glycogen, lactate and so on in high intensity exercise mice. The mice were divided into three groups; Normal Control (NC), Exercise Control (EC), and Exercise SQH (ES) by oral administered at 50mg/kg/day for 7 days. After excessive swimming,the ES group showed increases serum glucose and decrease serum lactate than EC group. Lactate content in muscle was lower ES group than EC group. Glycogen contents in muscle and liver were higher ES group than EC group. And, SQH administration increased the expression of phospho-Acetyl-CoA (p-ACC), and reduced the expression of phospho-AMP-activated protein kinase (p-AMPK) and GLUT4 in in-vivo model. Also, genome wide expression profiles of tissue were determined by RNA sequencing. SQH up-regulates and down-regulates several genes associated with fatigue. In conclusion, this study suggested that SQH are effective for anti-fatigue agent.
2021-04-24 | GSE113759 | GEO
Project description:Mesenchymal stromal cells (MSCs) are multipotent post-natal stem cells with applications in tissue engineering and regenerative medicine. MSCs can differentiate into osteoblasts, chondrocytes, or adipocytes, with functional differences in cells during osteogenesis accompanied by metabolic changes. The temporal dynamics of these metabolic shifts have not yet been fully characterized and are suspected to be of importance for therapeutic applications, such as osteogenesis optimization. Here, our goal was to characterize the metabolic shifts that occur during osteogenesis. We longitudinally profiled five key extracellular metabolites (glucose, lactate, glutamine, glutamate, and ammonia) from MSCs from four donors to classify osteogenic differentiation into three metabolic stages, defined by changes in the uptake and secretion rates of the metabolites in cell culture media. We used a combination of untargeted metabolomic analysis, targeted analysis of 13C-glucose labelled intracellular data, and RNA-sequencing data to reconstruct the gene regulatory network and further characterize cellular metabolism. The metabolic stages identified in this proof-of-concept study provide a framework for more detailed investigations aimed at identifying biomarkers of osteogenic differentiation and small molecule interventions to optimize MSC differentiation for clinical applications.
2021-12-20 | GSE191136 | GEO
Project description:Cloutier2009 - Brain Energy Metabolism
This model was taken from the
CellML
repository
and
automatically converted to SBML. Following the
submission the parameters are manually encoded and annotated as
spices and global quantities by BioModels curators.
The
original model was:
Cloutier M, Bolger FB, Lowry JP, Wellstead P. (2009) -
version=1.0
The
original CellML model was created by:
Catherine
Lloyd
c.lloyd@auckland.ac.nz
The
University of Auckland
This model is described in the article:
An integrative dynamic model
of brain energy metabolism using in vivo neurochemical
measurements.
Cloutier M, Bolger FB, Lowry JP,
Wellstead P.
J Comput Neurosci 2009 Dec; 27(3):
391-414
Abstract:
An integrative, systems approach to the modelling of brain
energy metabolism is presented. Mechanisms such as glutamate
cycling between neurons and astrocytes and glycogen storage in
astrocytes have been implemented. A unique feature of the model
is its calibration using in vivo data of brain glucose and
lactate from freely moving rats under various stimuli. The
model has been used to perform simulated perturbation
experiments that show that glycogen breakdown in astrocytes is
significantly activated during sensory (tail pinch)
stimulation. This mechanism provides an additional input of
energy substrate during high consumption phases. By way of
validation, data from the perfusion of 50 microM propranolol in
the rat brain was compared with the model outputs. Propranolol
affects the glucose dynamics during stimulation, and this was
accurately reproduced in the model by a reduction in the
glycogen breakdown in astrocytes. The model's predictive
capacity was verified by using data from a sensory stimulation
(restraint) that was not used for model calibration. Finally, a
sensitivity analysis was conducted on the model parameters,
this showed that the control of energy metabolism and transport
processes are critical in the metabolic behaviour of cerebral
tissue.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000554.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000554 | BioModels
Project description:This experiment was conducted to identify target genes of the peroxisome proliferator-activated receptor beta (PPARb) in skeletal muscle of transgenic mice that overexpressed PPARb. The following abstract from the submitted manuscript describes the major findings of this work. The Nuclear Receptor Transcription Factor PPARbeta/delta Programs Muscle Glucose Metabolism. Zhenji Gan, Eileen Burkart-Hartman, Dong-Ho Han, Brian Finck, Teresa C. Leone, John Holloszy, and Daniel P. Kelly. To identify new gene regulatory pathways controlling skeletal muscle energy metabolism, comparative studies were conducted on muscle-specific transgenic mouse lines expressing the nuclear receptors, PPARalpha (MCK-PPARalpha) or PPARbeta/delta (MCK-PPARbeta/delta). MCK-PPARbeta/delta mice are known to have enhanced exercise performance whereas MCK-PPARalpha mice perform at low levels. Transcriptional profiling revealed that the lactate dehydrogenase (Ldh)b/Ldha gene expression ratio is increased in MCK-PPARbeta/delta muscle, an isoenzyme shift that diverts pyruvate into the mitochondrion for the final steps of glucose oxidation. PPARbeta/delta gain- and loss-of-function studies in skeletal myotubes demonstrated that PPARbeta/delta, but not PPARalpha, interacts with the exercise inducible kinase, AMP-activated protein kinase (AMPK), to synergistically activate Ldhb gene transcription by cooperating with myocyte enhancer factor 2A (MEF2A), in a PPARbeta/delta ligand-independent manner. MCK-PPARbeta/delta muscle was shown to have high glycogen stores, increased levels of GLUT4, and augmented capacity for mitochondrial pyruvate oxidation suggesting a broad reprogramming of glucose utilization pathways. Lastly, exercise studies demonstrated that MCK-PPARbeta/delta mice had lower circulating levels of lactate compared to non-transgenic controls, while exhibiting supranormal performance on a high intensity exercise regimen. These results identify a transcriptional regulatory mechanism that increases capacity for muscle glucose utilization in a pattern that resembles the effects of exercise training. Keywords: muscle, exercise, nuclear receptors, glucose metabolism, gene regulation RNA from two wild-type (non-transgenic (NTG)) and two PPARbeta overexpressing (MCK-PPARb) mice was analyzed. Two replicates of each are provided.
2011-12-12 | E-GEOD-29055 | biostudies-arrayexpress
Project description:<p>Mass spectrometry imaging (MSI) visualises molecular distributions throughout tissues but is blind to dynamic metabolic processes. Here, MSI with high mass resolution together with multiple stable isotope labelling provided spatial analyses of phosphatidylcholine (PC) metabolism in mouse lungs. Dysregulated surfactant metabolism is central to many respiratory diseases. Metabolism and turnover of therapeutic pulmonary surfactants were imaged from distributions of intact and metabolic products of an added tracer, universally 13C-labelled dipalmitoyl PC (U[13C]DPPC). The parenchymal distributions of newly synthesised PC species were also imaged from incorporations of methyl-D9-choline. This dual labelling strategy demonstrated both lack of inhibition of endogenous PC synthesis by exogenous surfactant and location of acyl chain remodelling processes acting on the U[13C]DPPC-labelled surfactant, leading to formation of polyunsaturated PC lipids. This ability to visualise discrete metabolic events will greatly enhance our understanding of lipid metabolism in diverse tissues, and has potential application to both clinical and experimental studies. </p>
2020-10-30 | MTBLS2075 | MetaboLights
Project description:Experiment Description RNA sequencing was performed on Candida albicans wild type cells (SC5314) grown to exponential phase on YNB Lactate, YNB Glucose, or YNB Glucose plus Lactate, and compared to exponential Candida albicans crz1 cells grown on YNB Glucose or YNB Glucose plus Lactate. Three independent experiments were performed.
2016-10-03 | E-MTAB-4579 | biostudies-arrayexpress