ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Ahcy Acts as an Effector of Hnf4a-Driven Super-Enhancer Activation to Alleviate MASLD During Intermittent Fasting.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Intermittent fasting (IF) ameliorates metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanism remains unclear. Combined CUT&Run and transcriptomic analysis shows that hepatic Ahcy is controlled by the super‑enhancer (SE) and acts as a key mediator of IF's benefit. Liver‑specific Ahcy knockout worsens high‑fat diet (HFD)‑induced hepatic steatosis and blunts the protective effect of IF. Furthermore, inhibition of Brd4 or deletion of the core SE region reduces Ahcy expression and exacerbates lipid accumulation in vivo or in vitro. Hnf4a is identified as the transcription factor driving the Ahcy-SE. In vitro and in vivo experiments demonstrate that IF-activated Hnf4a directly binds to and activates the Ahcy-SE. Ahcy knockdown attenuates the lipid-deposition-reducing effect of Hnf4a overexpression in mice fed a HFD. In Ahcy
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