Summary of Study ST000428
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000332. The data can be accessed directly via it's Project DOI: 10.21228/M84G7M This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
Study ID | ST000428 |
Study Title | Targeted metabolomics of gastrocnemius tissue samples obtained from 20 month old (old) mice- Both Sham and after inducing lung injury (part II) |
Study Type | Targeted metabolomic analysis |
Study Summary | Introduction: Older patients are more likely to acquire and die from acute respiratory distress syndrome (ARDS) and muscle weakness may be more significant in older survivors. Recent data implicate muscle ring finger protein 1 (MuRF1) in lung injury-induced skeletal muscle atrophy in young mice and identify an alternative role for MuRF1 in cardiac metabolism regulation through inhibition of fatty acid oxidation. Objectives: To develop a model of lung injury-induced muscle wasting in old mice and to evaluate the skeletal muscle metabolomic profile of adult and old acute lung injury (ALI) mice. Methods: Young (2 month), adult (6 month) and old (20 month) male C57Bl6J mice underwent Sham (intratracheal H2O) or ALI [intratracheal E. coli lipopolysaccharide (i.t. LPS)] conditions and muscle functional testing. Metabolomic analysis on gastrocnemius muscle was performed using gas chromatography-mass spectrometry (GC-MS). Results: Old ALI mice had increased mortality and failed to recover skeletal muscle function compared to adult ALI mice. Muscle MuRF1 expression was increased in old ALI mice at day 3. Non-targeted muscle metabolomics revealed alterations in amino acid biosynthesis and fatty acid metabolism in old ALI mice. Targeted metabolomics of fatty acid intermediates (acyl-carnitines) and amino acids revealed a reduction in long chain acyl-carnitines in old ALI mice. Conclusion: This study demonstrates age-associated susceptibility to ALI-induced muscle wasting which parallels a metabolomic profile suggestive of altered muscle fatty acid metabolism. MuRF1 activation may contribute to both atrophy and impaired fatty acid oxidation, which may synergistically impair muscle function in old ALI mice. |
Institute | University of North Carolina;Duke University |
Department | UNC McAllister Heart Institute;Duke Molecular Physiology Institute |
Laboratory | Multiple Centers |
Last Name | Ilaiwy;WIllis |
First Name | Amro;Monte |
Address | 111 Mason Farm road, Chapel Hill, North Carolina, 27599-7126, USA |
monte_willis@med.unc.edu, amroilaiwy@gmail.com | |
Phone | 210-596-0171 |
Submit Date | 2016-07-05 |
Analysis Type Detail | GC-MS |
Release Date | 2016-09-23 |
Release Version | 1 |
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Combined analysis:
Analysis ID | AN000678 |
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Analysis type | MS |
Chromatography type | GC |
Chromatography system | Waters Acquity |
Column | Waters ACQUITY UPLC (1.7um) |
MS Type | EI |
MS instrument type | Single quadrupole |
MS instrument name | Agilent 5975 |
Ion Mode | POSITIVE |
Units | uM |