In a significant leap for diabetes research, scientists at the Mayo Clinic have developed a stem cell-based model that closely mimics the behavior of human pancreatic alpha cells under diabetic conditions. The findings, recently published in Stem Cell Reports, offer a powerful tool for understanding how alpha cells contribute to blood sugar dysregulation and for identifying potential new treatments.
According to the World Health Organization, more than 800 million people worldwide are currently living with diabetes—a chronic condition characterized by persistently high blood glucose levels. If left unmanaged, elevated blood sugar can cause widespread organ damage, reducing both quality of life and life expectancy.
Central to glucose regulation are the pancreas’s two main hormone-secreting cell types: beta cells, which lower blood sugar by releasing insulin, and alpha cells, which raise blood sugar by producing glucagon. A delicate balance between these two hormones is essential for maintaining metabolic stability.
While the role of beta-cell failure in diabetes has been extensively studied, mounting evidence suggests alpha cells are also significantly affected. However, a lack of robust lab-based models for human alpha cells has hindered efforts to explore their dysfunction in diabetic states—until now.
Dr. Quinn Peterson and his team have pioneered a method to generate functional human alpha cells from immature stem cells. These lab-grown alpha cells demonstrate striking similarities to their naturally occurring pancreatic counterparts, both in appearance and in their ability to secrete glucagon.
Crucially, when exposed to conditions that simulate the diabetic environment, these stem cell-derived alpha cells exhibited hallmark features of diabetes: excessive glucagon release and disrupted gene expression patterns. Notably, treatment with Sunitinib—an anti-cancer drug already approved for clinical use—successfully reversed the abnormal hormone secretion in the lab-grown cells.
This innovative model not only enhances our understanding of alpha cell behavior in diabetes but also provides a promising platform for screening potential therapeutics aimed at restoring proper glucagon regulation. As the global burden of diabetes continues to climb, such advances offer hope for more targeted and effective interventions.
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