Summary of Study ST000511

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR000383. The data can be accessed directly via it's Project DOI: 10.21228/M8JG7B This work is supported by NIH grant, U2C- DK119886.


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Study IDST000511
Study TitleDetermine how inhibition of autophagy/proteasome degradation or inhibition of protein synthesis in models of muscle insulin resistance affect amino acid metabolites
Study SummaryTo determine which protein degradation pathways downstream of IR and IGF1R contribute to changes in amino acid and mitochondrial metabolite pools, we will treat control, M-IR-/-, MIGIRKO, and HFD obese mice with inhibitors of autophagy or proteasome. We will treat 5 animals each of control, M-IR-/-, MIGIRKO, and HFD mice with vehicle, colchicine to inhibit autophagy, or MG132 to inhibit proteasome activity, then measure amino acid in muscle tissue.
Mayo Clinic
Last NameO'Neill
First NameBrian
AddressOne Joslin Place, Boston, MA 02215
Submit Date2016-11-18
Analysis Type DetailLC-MS
Release Date2018-12-11
Release Version1
Brian O'Neill Brian O'Neill application/zip

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Treatment ID:TR000547
Treatment Summary:Mice lacking insulin receptors (IR -/- genotype), or IGF-1 receptors (ICF-1 -/- genotype), or both were generated using Cre lox recombination. Controls were IR lox/lox, IGF-1 lox/lox, or both. Additional, 10 mice were included that were fed different diets for 8 weeks, chow or high fat diet.