June 09, 2016
Research led by Amnon Schlegel, M.D., Ph.D., Assistant Professor of Internal Medicine at the University of Utah School of Medicine and an Investigator with the University of Utah Molecular Medicine Program, reveals that defects in how the liver metabolizes glucose, caused by changes in the abundance of the FOXN3 protein, can also trigger increased blood sugar levels, and may explain why some individuals with a variation in the FOXN3 gene show signs of being at risk for diabetes.