Oliver's mTOR Atlas Evidence Platform
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Mechanisms of life span extension by rapamycin in the fruit fly Drosophila melanogaster

Bjedov I, Partridge L et al. · 2010 · Cell Metabolism · Atlas ID BJE2010

What this study shows

Feeding rapamycin extended fly lifespan through autophagy and reduced translation, and worked even in flies already on a lifespan-maximizing diet.

Abstract

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The target of rapamycin (TOR) pathway is a major nutrient-sensing pathway that, when genetically downregulated, increases life span in evolutionarily diverse organisms including mammals. The central component of this pathway, TOR kinase, is the target of the inhibitory drug rapamycin, a highly specific and well-described drug approved for human use. We show here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants. Increase in life span by rapamycin was associated with increased resistance to both starvation and paraquat.

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At a glance

Evidence type A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Drosophila melanogaster); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type4 - Animal Study
Model systemDrosophila melanogaster
JournalCell Metabolism
Year2010
Peer reviewedYes
Record last updated2026-08-22
SourceDOI 10.1016/j.cmet.2009.11.010 · PMID 20074526 · Free full text (PMC2824086)

Extracted findings

InterventionRapamycin (feeding)
TargetTOR
ModelDrosophila melanogaster
EffectFeeding rapamycin extends fly lifespan via autophagy and reduced translation
DoseRapamycin administered by feeding from early adulthood at 50, 200, and 400 μM; 200 μM produced the largest increase in median life span. Concentration in flies fed 200 μM food was 3.3 ± 0.2 ng/mg wet weight.
Sample sizeFlies of diverse genetic (w1118, yw, ovoD mutant) and cytoplasmic (Wolbachia-free) backgrounds, and both sexes were tested.
Effect sizeSignificant life span extension occurred at 50, 200, and 400 μM rapamycin, with 200 μM producing the largest increase in median life span. Rapamycin also significantly increased stress resistance (starvation, paraquat) and elevated triacylglyceride (TAG) levels, while reducing female fecundity in a dose-dependent manner.
Limitationsnot stated

In the Atlas

Related topics

LongevityRapamycinmTORC1Autophagy

Open questions that cite this study

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Cite this paper

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Bjedov, I., et al. (2010). Mechanisms of life span extension by rapamycin in the fruit fly Drosophila melanogaster. Cell Metabolism. https://doi.org/10.1016/j.cmet.2009.11.010

@article{BJE2010,
  author       = {Bjedov, I. and Partridge, L. and others},
  title        = {{Mechanisms of life span extension by rapamycin in the fruit fly Drosophila melanogaster}},
  journal      = {Cell Metabolism},
  year         = {2010},
  doi          = {10.1016/j.cmet.2009.11.010},
  note         = {PMID: 20074526},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper. 

Barton, O. (2026). Oliver's mTOR Atlas (record BJE2010) [Data set]. https://mtor-atlas.org/study/BJE2010/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_BJE2010,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record BJE2010},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/BJE2010/},
  doi          = {10.5281/zenodo.22059963}
}