Gökhan S. Hotamışlıgil
Leads a Harvard laboratory on metabolic disease and was elected to the US National Academy of Sciences in 2026 for achievements in metabolic research
James Stevens Simmons Professor of Genetics and Metabolism, Harvard T.H. Chan School of Public Health · Director, Center on Causes and Prevention of Cardiovascular Disease · Elected to the National Academy of Sciences (2026)
Portrait: Wikimedia Commons
KAL2026 asks how the liver switches on mTORC1 after a meal. Working in mouse models in which parts of the insulin pathway were removed from the liver, the authors found that insulin acts through AKT and the protein TSC2 to activate mTORC1, but that this route is not required for feeding to activate it. Dietary protein turns out to decide how much insulin signalling matters. Hotamışlıgil is the sixth of seven authors; Brendan Manning is the last author.
Hotamışlıgil is the James Stevens Simmons Professor of Genetics and Metabolism in the Department of Molecular Metabolism at the Harvard T.H. Chan School of Public Health, and he directs the Center on Causes and Prevention of Cardiovascular Disease. On 28 April 2026 the School announced his election to the National Academy of Sciences, citing distinguished and continuing achievements in metabolic research.
For the Atlas this paper is a reminder that mTORC1 in the liver listens to both hormones and food, and that the same pathway can be reached by more than one route.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Dietary protein governs the role of insulin signaling in the postprandial regulation of hepatic mTORC1. KAL2026 Sixth author of a mouse study showing that dietary protein governs whether insulin signalling is needed for postprandial activation of hepatic mTORC1. |
Co-authors in the Atlas
People with a profile here who share at least one study with Gökhan S. Hotamışlıgil.
- Brendan D. Manning Was among the groups that in 2002 identified TSC2 as a direct target of Akt, linking insulin and PI3K signalling to mTORC1, and later found TBC1D7 as the third subunit of the TSC complex. His lab has shown how mTORC1 turns growth signals into the synthesis of lipids and nucleotides
- Karen E. Inouye Metabolic physiologist who runs the Hotamışlıgil lab’s physiology facility, which specialises in glucose clamps, and co-authored two 2026 mouse studies on how feeding controls mTORC1 in liver and muscle.
- Krystle C. Kalafut Hepatic mTORC1 and nutrient signalling
- Madi Y. Cissé Research associate in the Manning lab and co-author on the two 2026 mouse studies showing which feeding signals switch on mTORC1 in liver and in skeletal muscle.
- Samuel C. Lapp First author of the muscle study showing that feeding-induced mTORC1 activation through AKT–TSC2 drives postprandial protein synthesis but is not needed to build or keep muscle mass.
- Yann Cormerais Research scientist in the Manning lab who works on how PI3K–AKT–TSC2 signalling controls mTORC1 in living tissues, using mouse models in which TSC2 cannot be phosphorylated by AKT.
Every researcher with a profile →
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