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Adv."],"published-print":{"date-parts":[[2026,9,25]]},"abstract":"<jats:p>\n                    The mechanistic target of rapamycin complex 1 (mTORC1) integrates nutrient and hormonal cues to regulate hepatic lipid metabolism with major implications for metabolic dysfunction-associated steatotic liver disease (MASLD). Here, we show that altered hepatic mTORC1\u2013TFEB\/TFE3 signaling is associated with coordinated remodeling of bile acid (BA) metabolism during metabolic adaptation. Our data support a model in which cross-talk between mTORC1 and TFEB\/TFE3 is associated with divergent regulation of bile acid synthesis and transformation. Depending on the mTORC1 signaling state, changes in hepatic\n                    <jats:italic toggle=\"yes\">Cyp2c70<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">Cyp8b1<\/jats:italic>\n                    expression, together with altered cholesterol trafficking, were associated with shifts toward non\u201312-OH or 12-OH bile acid species. These effects were attenuated or reversed by\n                    <jats:italic toggle=\"yes\">Tfe3<\/jats:italic>\n                    deletion or rapamycin treatment. Furthermore, protein restriction (which inhibits mTORC1) similarly reshaped the BA profile in mice and correlated with improved metabolic outcomes in MASLD patients. Together, these findings uncover BA homeostasis as an integral component of the metabolic adaptations orchestrated by mTORC1, underscoring a link between nutrient signaling and metabolic liver disease.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aee1905","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:58:53Z","timestamp":1790359133000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["mTORC1-TFEB\/TFE3 signaling is associated with bile acid diversification during hepatic metabolic adaptation"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-3924-4366","authenticated-orcid":true,"given":"Alex","family":"Zaufel","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz; Graz, Austria."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5762-6010","authenticated-orcid":true,"given":"Wenfei","family":"Sun","sequence":"additional","affiliation":[{"name":"Institute of Food, Nutrition and Health, ETH Zurich, Schwerzenbach, Switzerland."},{"name":"Division of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford University, Palo Alto, CA, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nunzia","family":"Pastore","sequence":"additional","affiliation":[{"name":"Telethon Institute of Genetics and Medicine (TIGEM); 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