Abstract
Is CYP2C70 the key to new mouse models to understand bile acids in humans?
Highlights
Humans and mice have substantially different bile acid (BA) pool compositions [1]
There has been considerable interest in the identity of the enzyme(s) responsible for converting chenodeoxycholic acid (CDCA) to muricholic acids (MCAs), the reason why rodents need this conversion for their physiology and metabolism, and whether we can make the mouse a better model to understand human BA metabolism and signaling
We know that synthesis of 6-hydroxylated BAs is mediated by a cytochrome P450, but identification of this enzyme remained a mystery until 2016, when Takahashi et al [2] reported that mice lacking the CYP2C family of enzymes were unable to synthesize MCAs, and CYP2C70 was identified as the likely CYP2C isoform responsible for 6-hydroxylation of CDCA to aMCA and ursodeoxycholic acid (UDCA) to bMCA
Summary
Humans and mice have substantially different bile acid (BA) pool compositions [1]. As the major primary BAs, humans synthesize cholic acid (CA) and chenodeoxycholic acid (CDCA), whereas mice have mainly CA and 6-hydroxylated muricholic acids (MCAs) that are made from CDCA (Fig. 1). There has been considerable interest in the identity of the enzyme(s) responsible for converting CDCA to MCAs, the reason why rodents need this conversion for their physiology and metabolism, and whether we can make the mouse a better model to understand human BA metabolism and signaling.
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