Benoit Viollet
Shows metformin still lowers blood sugar without AMPK or LKB1, redirecting the field toward a drop in cellular energy charge
Trained in Axel Kahn's lab, Institut Cochin de Génétique Moléculaire · shifted to AMPK biology late 1990s · now Directeur de Recherche (INSERM), Institut Cochin
Institut Cochin (INSERM/CNRS/Université Paris Cité) ↗
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 what let the 2011 ULK1 study (KIM2011) cleanly separate 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
| Year | Evidence | Study |
|---|---|---|
| 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 Contributes AMPK-knockout genetic tools letting the study cleanly show AMPK/mTORC1's opposing regulation of ULK1. |