In a study published Oct. 13 in Cell Metabolism, biologists at the University of Oregon and University of Utah report new insights into the microbiome-derived protein BefA that could lead to treatments for Type 1 diabetes, which affects millions of people worldwide.
UO biologist Karen Guillemin says these discoveries have “important, profound implications” that could lead to the development of new approaches to prevent diabetes by harnessing specific types of bacteria that produce BefA.
“If we understand how BefA works, it could give us a way to stimulate beta cell production therapeutically,” she said.
The paper’s first author is Jennifer Hampton Hill, who was a graduate student at the UO when she discovered that the BefA protein, made by gut bacteria, triggered insulin-producing cells to replicate. The protein was an important clue to the biological basis for Type 1 diabetes, an auto-immune disease in which the pancreas can’t make insulin. Hill is now a postdoctoral researcher at the University of Utah.