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
Institut Cochin, CNRS, Inserm, Université Paris Cité (papers 2010–2025) · Inserm U465, Centre de Recherches Biomédicales des Cordeliers, Paris (1999 paper)
Marc Foretz is first author of an Atlas study (FOR2010) that changed how scientists explain metformin, the most widely used diabetes drug. For years the simple story was that metformin works by switching on AMPK, the cell's energy sensor, which then shuts down sugar production in the liver. The team tested this in mice and liver cells that lacked AMPK or its activating kinase LKB1. Metformin still lowered glucose production. Instead, the drug lowered the liver's energy charge, the balance of ATP to its used-up forms, and that alone was enough to slow the making of new glucose.
For the Atlas this matters because metformin is often described as an indirect mTOR blocker acting through AMPK. The paper shows that its main sugar-lowering effect in the liver does not need that route, so any claim that metformin works mainly through AMPK and mTOR needs separate evidence. The experiments were in mice and isolated liver cells.
Foretz has worked on liver metabolism for more than 25 years. A 1999 paper from the Inserm unit at the Centre des Cordeliers in Paris, with Pascal Ferré and Fabienne Foufelle, showed that the transcription factor SREBP-1c carries insulin's message to genes for sugar and fat handling in liver cells. At the Institut Cochin, working closely with Benoit Viollet, Foretz went on to study AMPK and metformin in the liver, and in 2025 co-wrote a major review on how metformin lowers blood sugar. No official profile page could be opened, so the exact current title is not confirmed; the 2025 affiliation is the Institut Cochin.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| 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 First author: showed in mice and liver cells lacking AMPK or LKB1 that metformin still blocks glucose production by lowering the liver's energy charge. |
Co-authors in the Atlas 1
People with a profile here who share at least one study with Marc Foretz.
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- Benoit Viollet Showed that metformin still lowers liver glucose production without AMPK or LKB1, pointing instead to a drop in cellular energy charge
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