Constitutive mTORC1 Activation in Skeletal Muscle Increases Inflammation but is not Sufficient to Impair Glucose Tolerance.
What this study shows
Constitutive mTORC1 activation in mouse skeletal muscle (via GATOR1 complex KO) increases inflammatory markers but is not sufficient to impair glucose tolerance, indicating that additional metabolic inputs beyond muscle mTORC1 hyperactivation are required to drive glucose intolerance.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse |
| Journal | Function (Oxford, England) |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1152/function.039.2026 · PMID 42468920 · Free full text (PMC13459988) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Constitutive mTORC1 activation (GATOR1 muscle-specific KO) |
| Target | mTORC1 / GATOR1 complex |
| Model | Mouse |
| Effect | Increased skeletal muscle inflammation without impairment of glucose tolerance |
In the Atlas
Related topics
Open questions that cite this study
- Cited as supporting evidence for the open question Does mTORC1-selective dosing extend lifespan, and is rapamycin's glucose intolerance a cost at all?.
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- The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging (2016)
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