mTORC1 controls fasting-induced ketogenesis and its modulation by ageing
What this study shows
mTORC1 controls fasting-induced hepatic ketogenesis via PPARalpha, and this is blunted with age.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Mouse/cells) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Mouse/cells |
| Journal | Nature |
| Year | 2010 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/nature09584 · PMID 21179166 |
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 | Genetic (raptor liver knockout) |
| Target | mTORC1 / PPARα / ketogenesis |
| Model | Mouse/cells |
| Effect | mTORC1 controls fasting-induced ketogenesis (via PPARα); this control is blunted with ageing |
In the Atlas
Related topics
Links in the pathway map
- Supports Raptor required-for mTORC1
- Supports TSC1/TSC2 inhibits mTORC1
More studies on this topic
- AMPK phosphorylation of raptor mediates a metabolic checkpoint (2008)
- Architecture of human Rag GTPase heterodimers and their complex with mTORC1 (2019)
- Architecture of human mTOR complex 1 (2015)
- Tor forms a dimer through an N-terminal helical solenoid with a complex topology (2016)
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