UC Davis study points to potential of FGF21 in repairing livers

Yu-Jui Yvonne Wan

It turns out that mice are much better equipped than humans when it comes to regenerating and repairing the liver. A group of investigators at UC Davis note that the main difference is that rodents can rely on mouse PPARα that is much more efficient than human PPARα. And they've tested another protein, fibroblast growth factor 21 (FGF21), that could make up the difference for humans.

The team at UC Davis notes that they are building on an impressive research record for FGF21, which already includes evidence of spurring a tonic effect on insulin resistance, revving up fat metabolism and fighting fatty liver disease.

In their liver study they started with the observation that damaged livers in mice were quickly restored, even after more than half of the organ was removed by surgery. Mice with human PPARα, though, never fully healed--until FGF21 was added to the mix. And the study points the way to a new approach in treating damaged livers in humans.

"FGF21 is a key molecule to regulate metabolism in the liver," Yu-Jui Yvonne Wan, vice chair for research in the Department of Pathology and Laboratory Medicine at UC Davis and senior author on the paper. "There's research that shows that mice that overexpress FGF21 live 50 percent longer. Now we've shown that it can rescue human PPAR, allowing it to completely regenerate damaged livers in mice. This could provide significant therapeutic benefits for people after transplants or other liver injury."

The study was published in the journal Oncotarget.

- here's the release
- get the research paper

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