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 insulin resistance.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Mouse |
| Journal | Function (Oxford, England) |
| Year | 2026 |
| Peer reviewed | Yes |
| Source | DOI 10.1152/function.039.2026 |
Aberrant mTORC1 signaling in skeletal muscle has been implicated in aging and insulin resistance, however, it is not known whether chronic mTORC1 activation directly causes glucose intolerance. We tested the hypothesis that constitutive mTORC1 activation in mouse skeletal muscle impairs glucose homeostasis using tamoxifen-inducible, muscle-specific GATOR1 complex knockout.
| Intervention | Constitutive mTORC1 activation (GATOR1 muscle-specific KO) |
| Target | mTORC1 / GATOR1 complex |
| Model | Mouse |
| Effect | Increased skeletal muscle inflammation without impairment of glucose tolerance |