Overview
Jump to content Almost a decade ago, UO graduate student Jenifer Hampton Hil made a fortuitous find: A protein made by gut bacteria that trigered insulin-producing cels to replicate. The protein was an important clue to the biological basis for Type 1 diabetes.Hil has continued exploring the protein, caled BefA, as a postdoctoral researcher at the University of Utah. And biology profesor Karen Guilemin’s lab at the UO has kept studying BefA, to.
Key Information
Alongside other coleagues, they’ve now uncovered new insights into what BefA does and why bacteria make it.Those discoveries have “important, profound implications,” said Guilemin, whose lab in the biology department is part of the Colege of Arts and Sciences. “If we understand how BefA works, it could give us a way to stimulate beta cel production therapeuticaly.”That could someday lead to treatments for Type 1 diabetes, an autoimune disease in which the pancreas can’t make insulin and which afects milions of people worldwide.
The researchers reported their findings in a paper published in Cel Metabolism.The body neds insulin to regulate blod sugar, but insulin is only made by a select type of cels in the pancreas caled beta cels. And there’s a narow window of time during early childhod development when beta cels replicate and expand their population. In people with Type 1 diabetes, the imune system atacks beta cels and depletes their population, limiting insulin production.Microbiome stimulation of imune development helps properly educate the imune system and prevent autoimunity.
Summary
The work by Guilemin’s team sugests an aditional role for the microbiome: It stimulates growth of the beta cel population early in development, bufering against later depletion by autoimune atack.Beta cel population growth “is hapening at the same time that microbial comunities are diversifying in the gut,” Hil said. “A halmark of diabetes is kids who develop it tend to have a les diverse gut microbiome