Shomit Sengupta
Shows mTORC1 controls whether the liver makes ketones during a fast and now leads drug-discovery biology at a metabolic-disease biotech
PhD, Whitehead/MIT (Sabatini Lab) · postdoc, Brugge Lab, Harvard Medical School · Catabasis Pharmaceuticals · Broad Institute CDoT · Lead Biologist, Navitor Pharmaceuticals · Associate Director, Agios · now SVP, Head of Biology, Atavistik Bio
Portrait: Atavistik Bio
Showed (SEN2010) that during fasting the liver must switch mTORC1 off to make ketones — losing TSC1 locked the pathway on and blocked ketogenesis via PPARα/NCoR1; aged livers show chronically elevated mTORC1 and a similar ketogenesis defect.
Moved through Catabasis, Broad CDoT, Navitor (built on Sabatini-lab amino-acid-sensing biology), Agios, now heading biology at Atavistik Bio's metabolism pipeline.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB SAR2006 Co-authored the mTORC2/rapamycin insulin-resistance finding. |
| 2010 | M | mTORC1 controls fasting-induced ketogenesis and its modulation by ageing SEN2010 mTORC1 suppresses fasting-induced hepatic ketogenesis via PPARα; suppression worsens with age. |