Microbial origins of Type 1 diabetes: A bacterial protein triggers insulin-producing cells to reproduce, pointing to a possible treatment

Almost a decade ago, UO graduate student Jennifer Hampton Hill made a fortuitous find: A protein made by gut bacteria that 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 has continued researching this protein, called BefA, as a postdoc at the University of Utah. And Karen Guillemin’s lab at UO has kept studying BefA, too. Alongside other colleagues, they’ve now uncovered new insights into what BefA does and why bacteria make it.

Those discoveries have “important, profound implications,” said Guillemin. “If we understand how BefA works, it could give us a way to stimulate beta cell production therapeutically.” That could someday lead to treatments for Type 1 diabetes, which affects millions of people worldwide.

The researchers reported their findings in a paper published October 13 in Cell Metabolism.

The body needs insulin to regulate blood sugar, but insulin is only made by a select type of cells in the pancreas called beta cells. And there’s a narrow window of time during early childhood development when beta cells replicate and expand their population. In people with Type 1 diabetes, the immune system attacks beta cells and depletes their population, limiting insulin production.

Microbiome stimulation of immune development helps properly educate the immune system and prevent autoimmunity. Guillemin’s team’s work suggests an additional role for the microbiome: It stimulates growth of the beta cell population early in development, buffering against later depletion by autoimmune attack.

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