Abstract: For decades, diabetes research leaned heavily on rodent models, and while they taught us a lot, they also misled us just enough to stall real breakthroughs. Today, thanks to massive human biobanks like nPOD, HPAP, and the Exeter Archival Diabetes Biobank, the science world is finally peering directly into the human pancreas rather than guessing from mice. This shift has opened the door to multiomic profiling, spatial analysis, electrophysiology, and computational genomics that reveal the full complexity of Type 1 diabetes as it unfolds in real human tissues. The latest study by dos Santos and colleagues shows just how powerful this approach is, uncovering unexpected dysfunction not just in β cells, the usual suspects but also in α cells, which become hyperactive and lose their regulatory balance early in disease.
What makes this discovery compelling is how biobank-driven research helps scientists compare real donor islets at different disease stages, revealing patterns that animal models could never capture. The α cells, long overshadowed by their β cell counterparts, now emerge as active players shaped by genetics, immune exposure, and cellular stress. Their resilience surviving years of inflammation that destroy β cells opens new therapeutic possibilities. But this progress also highlights the challenges of human-based research: limited tissue availability, donor variability, and the inability to track changes longitudinally. Yet with biobanks, stem cell derived islets, advanced imaging, and humanized mice, the field is stepping into a new era, one where diabetes is studied at human depth, not rodent distance.
Get the full article here: https://pmc.ncbi.nlm.nih.gov/articles/PMC12646651/
