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New horizons in the regulation of bile acid and lipid homeostasis: critical role of the nuclear receptor FXR as an intracellular bile acid sensor
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Bile acids (BA) play an important role in human
physiology.1 As amphipathic water soluble end products of
cholesterol metabolism, they participate in body cholesterol disposal
as well as generation of bile flow and biliary lipid secretion.
However, in spite of being key endobiotics, BA are intrinsically toxic
for cells mainly because of their inherent detergent and membrane
disruptive properties. In fact, BA induced hepatotoxicity has been
implicated in the pathogenesis and perpetuation of liver injury in
cholestatic liver diseases.2 Therefore, it is not
surprising that intracellular BA levels are tightly maintained within a
narrow concentration range3 as too much leads to
hepatotoxicity while too little can lead to significant impairments in
bile flow and luminal fat digestion. How the liver orchestrates the
regulation of intracellular BA concentrations appears to be through
transcriptional regulation of genes involved in both BA biosynthesis
and transport. The recent cloning and identification of major
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