New study targets molecular culprit of liver disease

Petra Fromme directs the Biodesign Center for Applied Structural Discovery

Some 80-100 million people in the US have a serious medical condition known as non-alcoholic fatty liver disease (NAFLD). The affliction is caused by abnormal retention of fat within cells or organs. People of all ages are vulnerable to this disease, though individuals suffering from obesity or type 2 diabetes are at heightened risk.

Michael Moran is a researcher in the Biodesign Center for Applied Structural Discovery and ASU's School of Molecular Sciences. he is the first author of the new study.

In a new study, researchers at the Biodesign Center for Applied Structural Discovery (CASD) and their colleagues use NMR technology to probe a protein known as known as G0S2. By understanding the molecular structure in minute detail, researchers hope to develop drugs capable of targeting this protein and alleviating symptoms of NAFLD or perhaps, preventing the disease altogether.

The CASD research team, under the directorship of co-author Petra Fromme, is joined by colleagues from the Biodesign Center for Innovations in Medicine, ASU’s School of Molecular Sciences and researchers at Mayo Clinic, Scottsdale.

Elizabeth Paige Ramirez, currently Clinical Study Manager at Celerion was a researcher at the Biodesign Center for Applied Structural Discovery and ASU's School of Molecular Sciences. She is second author of the new study.

According to lead author Michael Moran: "G0S2 is a recently discovered protein involved in non-alcoholic fatty liver disease and I am so excited to share with the world information that can aid in the discovery not only of a structure of this protein, but also potential treatment for those affected by this illness."

Further structural studies of G0S2 offer hope for better addressing NAFLD, the most prevalent form of chronic liver disease, for which no FDA approved treatments currently exist.

The research appears in the current issue of the journal PLOS ONE.

Richard Harth