Summary of Study ST003241
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 PR002013. The data can be accessed directly via it's Project DOI: 10.21228/M8DJ7S This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST003241 |
| Study Title | Lipidomic analysis of lung from Gclc WT and whole-body Gclc KO mice. |
| Study Summary | We found decreased levels of triglycerides in the lung of whole-body deletion of Gclc mice compared to wildtype mice. |
| Institute | University of Rochester Medical Center |
| Last Name | Harris |
| First Name | Isaac |
| Address | 601 Elmwood Ave, Rochester, New York, 14642-0001, USA |
| isaac_harris@urmc.rochester.edu | |
| Phone | 8572348624 |
| Submit Date | 2024-05-29 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2024-06-07 |
| Release Version | 1 |
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Project:
| Project ID: | PR002013 |
| Project DOI: | doi: 10.21228/M8DJ7S |
| Project Title: | Glutathione synthesis in the mouse liver supports lipid abundance through NRF2 repression. |
| Project Summary: | Cells rely on antioxidants to survive. The most abundant antioxidant is glutathione (GSH). The synthesis of GSH is non-redundantly controlled by the glutamate-cysteine ligase catalytic subunit (GCLC). GSH imbalance is implicated in many diseases, but the requirement for GSH in adult tissues is unclear. To interrogate this, we have developed a series of in vivo models to induce Gclc deletion in adult animals. We find that GSH is essential to lipid abundance in vivo. GSH levels are highest in liver tissue, which is also a hub for lipid production. While the loss of GSH does not cause liver failure, it decreases lipogenic enzyme expression, circulating triglyceride levels, and fat stores. Mechanistically, we find that GSH promotes lipid abundance by repressing NRF2, a transcription factor induced by oxidative stress. These studies identify GSH as a fulcrum in the liver's balance of redox buffering and triglyceride production. |
| Institute: | University of Rochester Medical Center |
| Last Name: | Harris |
| First Name: | Isaac |
| Address: | 601 Elmwood Ave, Rochester, New York, 14642-0001, USA |
| Email: | isaac_harris@urmc.rochester.edu |
| Phone: | 8572348624 |
