Experts at the University of Pennsylvania School of Medicine claim that their finding suggests that FOXA2 may become the focus for new therapies to treat diseases that involve the regulation of bile salts.
After its formation in the liver, bile gets stored in the gall bladder, and transported through ducts to the small intestine where it helps to digest fats from food.
Chemicals in bile that help digest fats and keep cholesterol dissolved are called bile salts. The liver maintains their balance by degrading old bile salts and synthesizing new ones.
Problems arise when too many bile salts accumulate in the liver.
The researchers say that diseases of bile regulation, like primary sclerosing cholangitis (PSC), are characterized by problems with bile transport from the liver to the gut.
In children with biliary atresia and adults with PSC, they have found that the expression of FOXA2 in the liver is severely reduced.
According to them, FOXA2 regulates the expression of transporter proteins that are responsible for moving bile out of the liver, as well as several enzymes that function in bile acid detoxification.
Based on their observations, the researchers came to the conclusion that low FOXA2 levels exacerbate liver injury.
The researchers believe that medications or DNA therapies that increase the expression of FOXA2 in liver cells may offer a new means of treating PSC and other similar syndromes.
"In order to lay the groundwork for developing new treatments, we have to determine how FOXA2 itself is regulated," Nature magazine quoted first author Irina Bochkis, a doctoral student in Genomics and Computational Biology, as saying.