The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging

Kennedy BK, Lamming DW · 2016 · Cell Metabolism · Atlas ID KEN2016

What this study shows

A Cell Metabolism review framing mTOR as the 'grand conductor' that coordinates whole-body metabolism, tissue by tissue. Especially valuable for its clear-eyed section on WHY rapamycin causes metabolic side effects (the mTORC2 problem) - which is the main barrier to using it against aging. Pairs perfectly with Lamming's own 2012 mechanism paper.

Abstract

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Since the discovery that rapamycin, a small molecule inhibitor of the protein kinase mTOR (mechanistic target of rapamycin), can extend the lifespan of model organisms including mice, interest in understanding the physiological role and molecular targets of this pathway has surged. While mTOR was already well known as a regulator of growth and protein translation, it is now clear that mTOR functions as a central coordinator of organismal metabolism in response to both environmental and hormonal signals.

Read the full abstract on PubMed →

At a glance

Evidence type	R Review — secondary literature, not a new result Marked R because it is a review or synthesis of existing evidence rather than a new primary result; that is a different form of writing, not a weaker one.
Study type	Narrative Review
Model system	Review (metabolism/aging)
Journal	Cell Metabolism
Year	2016
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1016/j.cmet.2016.05.009 · PMID 27304501 · Free full text (PMC4910876)

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	Not applicable (review)
Target	mTOR
Model	Review
Effect	Reviews mTOR as a central coordinator of organismal metabolism and aging

In the Atlas

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?.

Cite this paper

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Kennedy, B. K., & Lamming, D. W. (2016). The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging. Cell Metabolism. https://doi.org/10.1016/j.cmet.2016.05.009

@article{KEN2016,
  author       = {Kennedy, B. K. and Lamming, D. W.},
  title        = {{The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging}},
  journal      = {Cell Metabolism},
  year         = {2016},
  doi          = {10.1016/j.cmet.2016.05.009},
  note         = {PMID: 27304501},
}

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 KEN2016) [Data set]. https://mtor-atlas.org/study/KEN2016/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_KEN2016,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record KEN2016},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/KEN2016/},
  doi          = {10.5281/zenodo.22059963}
}

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