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This pharmacologic feature is directly relevant to hepatic impairment because the drug's efficacy does not depend on liver enzyme function for activation

The metabolism of BA after MBS is not fully known, but it is recognised that they act on cells in the intestinal wall by activating the farnesoid x receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5), which potentiates the release of GLP-1 [12]

Pre-treatment of rats with 120 g/kg DSIP 20 minutes prior to subjection to hypoxia completely inhibited these hypoxia-induced reductions in mitochondrial respiratory activity

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parkeri to avoid ubiquitin targeting and restriction by antibacterial autophagy R

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