Table 1.

Regulatory effects of bile acids.

Effect	Bile acids*	Human Receptor(s)/Mechanism
Detoxification/excretion of xenobiotic compounds and LCA (Xie et al. 2001; Staudinger et al. 2001; Sonoda et al. 2002)	LCA	steroid and xenobiotic receptor (SXR) pregnane X receptor (PXR)
Detoxify LCA (Makishima et al. 2002; Ishizawa et al. 2008)	LCA & derivatives	vitamin D receptor (VDR)
Mobilize intracellular calcium (Voronina et al. 2002; Fischer et al. 2007; Nguyen and Bouscarel 2008)	(T)CDCA TCA (T)DCA TLCA TLCA-S TUDCA	phosphatidylinositol 3-kinase (PI3K) inositol triphosphate (IP3) ryanodine receptors (RyRs)
Stimulatation/inhibition of cAMP synthesis (tissue-specific effects) (Bouscarel et al. 1995; Bouscarel et al. 1999; Chignard et al. 2003; Keitel et al. 2007; Nguyen and Bouscarel 2008)	(T)CDCA TCA (T)DCA TLCA (T)UDCA UCA	glucagon protein kinase C (PKC) G-protein coupled receptor (TGR5)
PKC activation and translocation (Beuers et al. 1999; Lau et al. 2005; Looby et al. 2005; Shah et al. 2005; Le et al. 2006; Nguyen and Bouscarel 2008)	(G)CDCA (T)CA DCA TLCA (T)UDCA	unknown†
Induction of expression of interleukin 1 (IL-1) and tumor necrosis factor alpha (TNFα) (Miyake et al. 2000)	CDCA	interaction with Kupffer cells
Production of reactive oxygen species (ROS)(Fang et al. 2004)	(T)DCA	induction of mitochondria

^*Bile acids known to be associated with the effect. Conjugates in parenthesis indicate both the conjugated and deconjugated bile acid have effect.

^†Unknown if reaction is direct or receptor-mediated.