Benoit Viollet
Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
Directeur de Recherche (INSERM), Institut Cochin · shifted to AMPK biology late 1990s · trained in Axel Kahn's lab, Institut Cochin de Génétique Moléculaire
Institut Cochin (INSERM/CNRS/Université Paris Cité) (Paris, France) ↗ ORCID0000-0002-0121-0224 ↗
Portrait: Institut Cochin
In 2010 (FOR2010), using AMPK/LKB1-knockout mice and hepatocytes, showed metformin still suppresses hepatic glucose production — contradicting the standard AMPK-dependent model, pointing instead to a drop in energy charge. His AMPK-knockout genetic tools were used in the 2011 ULK1 study (KIM2011), which separated AMPK's activating vs. mTORC1's inhibitory phosphorylation of ULK1.
Began career in liver gene transcription (Axel Kahn lab), then built AMPK-subunit knockout mouse lines used field-wide for two decades. Nutrition Research Award (2000), Institut Benjamin Delessert Prize (2004), Descartes-Huygens Prize (2015).
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2010 | M | Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy EGA2010 AMPK directly phosphorylates ULK1 to connect energy sensing to autophagy/mitophagy, opposing mTOR. |
| 2010 | M | Metformin, independent of AMPK, inhibits mTORC1 in a rag GTPase-dependent manner KAL2010 Metformin inhibits mTORC1 even in cells lacking AMPK or TSC1/TSC2, and the effect requires the Rag GTPases instead. Together with Foretz 2010 this places a large part of metformin's action outside the AMPK axis it is usually credited to. |
| 2010 | A | Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state FOR2010 Metformin still suppresses hepatic glucose production without AMPK or LKB1. |
| 2011 | M | AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 KIM2011 Contributed AMPK-knockout genetic tools to the study showing AMPK/mTORC1's opposing regulation of ULK1. |
Co-authors in the Atlas 14
People with a profile here who share at least one study with Benoit Viollet.
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- Mondira Kundu 2 shared studies Physician-scientist who works out what the autophagy-initiating kinases ULK1 and ULK2 actually do when a cell runs short of fuel
- Adem Kalender Cell biologist who, in George Thomas's group at the University of Cincinnati, showed that metformin can switch off mTORC1 without AMPK by acting through the Rag GTPases
- Dana M. Gwinn First author of the 2008 study showing that the energy sensor AMPK switches off mTORC1 by phosphorylating raptor
- Daniel F. Egan Showed as first author that AMPK directly phosphorylates ULK1, linking low cellular energy to autophagy and mitophagy, and contributed to the finding that AMPK brakes mTORC1 by phosphorylating raptor
- David B. Shackelford Cancer biologist at UCLA who studies lung tumours that have lost the LKB1 tumour suppressor, the upstream activator of AMPK, and who trained in Reuben Shaw's lab at the Salk Institute
- George Thomas Purified and cloned S6K1, the kinase that became the classic readout of mTORC1 activity. His lab later showed that mice lacking S6K1 resist diet-induced obesity, and that amino acids signal to mTORC1 through the lipid kinase hVps34 (GUL2008)
- John M. Asara Mass-spectrometry specialist whose core facility supplied metabolomics and proteomics for several mTOR studies, including measurements of purine, pyrimidine and SAM metabolism downstream of mTORC1.
- Joungmok Kim Showed as a Guan-lab postdoc that AMPK and mTORC1 control autophagy by phosphorylating ULK1 at different sites, with mTORC1's mark on Ser757 blocking activation by AMPK
- Kun-Liang Guan Showed how growth-factor and energy signals reach mTORC1 through TSC2 and Rheb, and, in parallel with the Sabatini lab, that the Rag GTPases carry the amino-acid signal. His lab also found that AMPK and mTORC1 control autophagy by phosphorylating the kinase ULK1 at different sites
- Malene Hansen Showed in worms, alongside a 2007 report from Beth Levine's laboratory, that autophagy is required for dietary restriction to extend lifespan
- Marc Foretz Researcher at the Institut Cochin in Paris who studies how the liver controls sugar and fat, and whose 2010 work showed that metformin can lower liver glucose output without AMPK
- Maria M. Mihaylova Studies how intestinal stem cells change with age and how diet shapes their metabolism
- Reuben J. Shaw Showed, in parallel with two other groups, that the tumour suppressor LKB1 directly activates AMPK, and that AMPK brakes mTORC1 by phosphorylating raptor. His Salk lab also linked AMPK to autophagy through ULK1 and helped explain how metformin acts in the liver
- Sara C. Kozma Studies the S6K/mTOR pathway and how it controls cell growth, ribosome production, diabetes and cancer, including mTOR signalling in liver cancer.
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