At its most fundamental level, diabetes is a disease characterized by stress -- microscopic stress that causes inflammation and the loss of insulin production in the pancreas, and system-wide stress due to the loss of that blood-sugar-regulating hormone.
Now, researchers led by scientists at the University of California, San Francisco (UCSF) have uncovered a new key player in amplifying this stress in the earliest stages of diabetes: a molecule called thioredoxin-interacting protein (TXNIP). The molecule, they've discovered, is central to the inflammatory process that leads to the death of the cells in the human pancreas that produce insulin.
"This molecule does something remarkable -- it takes stress and makes it worse," said the senior author of the study, UCSF's Feroz Papa, MD, PhD, an associate professor of medicine at UCSF and a member of the UCSF Diabetes Center and the California Institute for Quantitative Biosciences (QB3).
The study is published this week in the journal Cell Metabolism, with a parallel study by researchers at Washington University in St. Louis. Both studies were funded by the Juvenile Diabetes Research Foundation (JDRF).
The work provides a roadmap for finding new drugs that could target and shut down the action of TXNIP, thus preventing or stalling the inflammatory processes it amplifies. Researchers in the field believe that this strategy could benefit people in the early days of the disease, when diabetes is first developing or is soon to develop -- a time referred to as the "honeymoon" period.
Clinical studies have already shown that dietary changes and other approaches can extend the honeymoon period in some people and prevent diabetes in others. The overarching goal of Papa's research, he said, is to find a way to extend this honeymoon period indefinitely.
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University of California - San Francisco