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Farnesoid X receptor-induced lysine-specific histone demethylase reduces hepatic bile acid levels and protects the liver against bile acid toxicity.


ABSTRACT:

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Bile acids (BAs) function as endocrine signaling molecules that activate multiple nuclear and membrane receptor signaling pathways to control fed-state metabolism. Since the detergent-like property of BAs causes liver damage at high concentrations, hepatic BA levels must be tightly regulated. Bile acid homeostasis is regulated largely at the level of transcription by nuclear receptors, particularly the primary BA receptor, farnesoid X receptor, and small heterodimer partner, which inhibits BA synthesis by recruiting repressive histone-modifying enzymes. Although histone modifiers have been shown to regulate BA-responsive genes, their in vivo functions remain unclear. Here, we show that lysine-specific histone demethylase1 (LSD1) is directly induced by BA-activated farnes

SUBMITTER: Kim YC 

PROVIDER: S-EPMC4480214 | biostudies-literature | 2015 Jul

REPOSITORIES: biostudies-literature