Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity
What this study shows
S6K1 deletion protects mice from age- and diet-induced obesity and enhances insulin sensitivity.
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 (S6K1 KO)); 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 (S6K1 KO) |
| Journal | Nature |
| Year | 2004 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/nature02866 · PMID 15306821 |
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 – S6K1 knockout |
| Target | S6K1 (downstream of mTORC1) |
| Model | Mouse (S6K1 KO) |
| Effect | S6K1 loss protects against age- and diet-induced obesity and enhances insulin sensitivity |
In the Atlas
Related topics
Links in the pathway map
- Supports S6K1 inhibits IRS-1 / IRS-2
More studies on this topic
- Inferring feedback regulation from static snapshots of a single signal (2026)
- Inappropriate activation of the TSC/Rheb/mTOR/S6K cassette induces IRS1/2 depletion, insulin resistance, and cell survival deficiencies (2004)
- The TSC1-2 tumor suppressor controls insulin-PI3K signaling via regulation of IRS proteins (2004)
- mTOR inhibition induces upstream receptor tyrosine kinase signaling and activates Akt (2006)
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