Endocrinology

The Future of Type 1 Diabetes Management

The future of type 1 diabetes management may involve more than just insulin. (Stock photo)

Think type 1 diabetes (T1D), and you think of insulin. You think incurable. You think forever. But the introduction of the first disease-modifying drug, the immunomodulator teplizumab, along with investigational approaches such as beta-cell preservation, gene editing and stem cell therapy, show that what we thought was the final word was really just the opening argument.

“For so long, we treated type 1 diabetes symptomatically with insulin alone, which is absolutely essential and life-saving,” Children’s of Alabama pediatric endocrinologist Ambika P. Ashraf, M.D., said. “But if we recognize it as an autoimmune disease, then we need to treat the immune process driving it, not just the high blood sugars. You don’t treat rheumatoid arthritis by just controlling inflammation alone,” she said.

To highlight where the field is at this important point in time, Ashraf co-edited a journal supplement, a special collection of research articles on T1D, in Frontiers in Endocrinology.

The supplement, published as a collection of 14 peer-reviewed articles, brings together researchers from around the world to address immune modulation, beta-cell preservation, remission, screening, gene editing, stem cell therapies and metabolic memory. The goal was not to champion one therapy, Ashraf said, but to show how the future of type 1 diabetes care will be built from complementary approaches to slow, stop or even prevent disease progression.

Two articles are authored by researchers at Children’s and the University of Alabama at Birmingham (UAB).

“When you look at all this work together as a collection, you start thinking about different ways to approach the management of type 1 diabetes,” she said.

The idea emerged while Ashraf and her colleagues were outlining a chapter on disease-modifying therapy for a pediatric diabetes textbook. “There was simply too much important work happening,” she said. “It became clear that disease-modifying approaches in type 1 diabetes deserved a deeper, more focused conversation.”

When Frontiers invited proposals for a themed issue, the timing was perfect.

“We knew this was it—bringing together the growing body of research that is shifting type 1 diabetes from a condition we only manage to one we may be able to change, delay or even prevent,” she said.

The supplement focuses on three questions: Can we slow or stop the immune destruction of beta cells? Can we preserve insulin production?  Can we delay or prevent the onset of symptomatic type 1 diabetes?”

“Remission is so important because if you stop autoimmunity, then you can get back to having normal function,” she said. At the same time, beta cell preservation is also key. “They go hand in hand.”

Another theme in the supplement is screening for antibodies that predict type 1 diabetes risk before symptoms appear, which opens the door to interventions when they are most beneficial. But universal screening is only practical if therapies are effective and accessible, Ashraf said. “If we had a medication that we could confidently say, ‘Take this, and it would reliably reduce your risk of developing T1D,’ then universal screening would be transformative,” she added.

Several articles in the collection explore therapies that support beta‑cell health without suppressing the immune system but by strengthening the cells themselves. These include medications like verapamil, experimental TXNIP‑targeting drugs and high‑dose GABA, all of which aim to help insulin‑producing cells survive longer.

Perhaps the most important message of the supplement is that there likely will not be a one-size-fits-all approach for people with T1D, but a mix of options based on the individual patient. As Ashraf and her co-editors wrote in an editorial in the issue: “The innovative concepts highlighted here will undoubtedly shape the future of diabetology and inspire further research into state-of-the-art, disease-modifying therapies for T1D.”

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