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Studies suggest promising new directions for gallstone treatment

ontrols genes whose proteins regulate the transport of bile acids and phospholipids from the liver into the gallbladder. Previous studies had indicated that FXR's activity is low in strains of mice that are more susceptible to gallstone disease.

To study FXR's function, the researchers used a knockout mouse that lacked the FXR gene. They then fed the mice a "lithogenic" diet, which is designed to induce gallstone formation because it is high in cholesterol and other components of bile.

Mice are good models for CGD, said Mangelsdorf, because mice and humans have the same genetic regulatory pathways to control the components of bile. Also, the mouse version of CGD physiologically mimics the disease that is observed in humans.

The researchers' analyses of bile components in the knockout mice revealed cholesterol saturation and lower levels of biliary lipids, resulting in cholesterol crystals -- conditions that closely matched those seen in humans with CGD. They also found that the bile acids created the same hydrophobic conditions and inflammation that are hallmarks of the human disease.

Finally, the researchers measured the activity of genes known to be regulated by FXR in the knockout mice. Among these, they found low activity in those involved in the transportation of lipid components of bile.

"Once we had established that the FXR-deficient animals were much more susceptible than normal animals to getting all the sequelae of CGD, we decided to explore the effects of enhancing FXR activity in a strain of mouse that was known to have FXR, but which was also susceptible to the disease," said Mangelsdorf. "We wanted to determine whether such a drug could reestablish the proper equilibrium of the bile components."

To do this, the researchers gave CGD-susceptible mice, which were fed a lithogenic diet, a synthetic compound, code-named GW4064, which is known to mimic the natural chemical that switches on FXR. GW4064 is
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
22-Nov-2004


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