A new study from the University of California, Davis, has uncovered how cells in the pancreas work together to stop blood sugar from dropping too low.
This discovery could lead to better treatments for people with diabetes, helping them avoid dangerous episodes of low blood sugar, also known as hypoglycemia.
People with diabetes already face long-term risks from high blood sugar, such as vision problems, kidney failure, and nerve damage.
But they also face a more immediate threat: sudden drops in blood sugar caused by insulin or other medications. These drops can lead to unconsciousness, coma, or even death if not treated quickly.
Mohammad Pourhosseinzadeh, a medical and Ph.D. student at UC Davis, worked with Professor Mark Huising to study how the body normally prevents low blood sugar. They discovered that a group of rare cells in the pancreas, called delta cells, play a key role in this process.
The pancreas contains small clusters of cells known as the Islets of Langerhans. Most attention has gone to the beta cells in these clusters, which make insulin. But the delta cells, which make up only about 5% of the islet cells, were not well understood until recently.
When blood sugar rises, the beta cells release insulin in pulses. These insulin pulses also release a second hormone called urocortin-3. In earlier research, Huising found that urocortin-3 tells delta cells to release somatostatin, a hormone that signals beta cells to take a break from making insulin.
This feedback loop helps the body avoid sending out too much insulin, which would lower blood sugar too much. In mice that lacked delta cells, blood sugar levels stayed too low because there was no somatostatin to signal a pause in insulin production.
The researchers also found that people with diabetes have lower levels of urocortin-3, which could explain why they are more at risk for hypoglycemia.
In the new study, the team looked at how beta and delta cells coordinate with each other. They found that both types of cells pulse together in rhythm, like dancers moving in sync.
These signals travel through tiny connections called gap junctions, made from a protein called connexin 36. If these connections were blocked, the delta cells could not respond properly, even when they received urocortin-3.
Pourhosseinzadeh explained that the communication between these cells happens in two steps: First, the gap junctions quickly alert the delta cells to get ready. Then, about 30 seconds later, urocortin-3 boosts the response, leading to the release of somatostatin and a pause in insulin release.
This teamwork between beta and delta cells may hold the key to preventing hypoglycemia in people with diabetes. By restoring this 1-2 communication system, future drugs could work better and make diabetes treatments safer.
The team now plans to study how this process can be used to improve current medications. They hope this discovery will lead to new strategies to protect people with diabetes from sudden and life-threatening drops in blood sugar.
If you care about diabetes, please read studies about New diabetes drug could control blood sugar and body weight better and findings of Common diabetes drugs linked to increased heart risk.
For more about diabetes, please read studies about Why diabetes drug metformin can help increase longevity and findings of This drug could manage type 2 diabetes for a long time.
The study is published in PNAS.
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