Scientists at City of Hope have identified a gene with a surprising link to type 2 diabetes (T2D). The gene, known as SMOC1, appears to disrupt normal pancreatic cell function — instead of lowering blood sugar, these cells begin to raise it.
This breakthrough offers new insight into how T2D develops and could pave the way for innovative treatment options in the future.
New findings could pave the way for better treatment, diagnosis, and prevention of type 2 diabetes (T2D). Published in Nature Communications, the study explored why insulin‑producing cells in the pancreas stop working properly in people with diabetes.
The pancreas contains clusters of cells called islets. Normally, beta cells make insulin to lower blood sugar, while alpha cells produce glucagon to raise it — keeping blood sugar in balance. In T2D, that balance is disrupted as some beta cells lose their identity and start acting like alpha cells, producing glucagon instead of insulin.
To investigate, scientists analyzed islet cells from 26 people (half with T2D) using RNA sequencing. They discovered that in healthy individuals, cells remained flexible, maturing into either alpha or beta cells. But in diabetes, this flexibility was lost — beta cells only shifted into alpha cells, never the reverse. This one‑way change helps explain why insulin drops while glucagon rises in T2D.
This research does give hope that by targeting the root causes of type 2 diabetes at the genetic level, new treatments may one day be able to help millions of people better manage or even reverse their condition.
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