JOIN USA team at John Hopkins University claims that the finding solves a longtime mystery and would provide for the first time an explanation of the process of insulin secretion, the 'Cell Metabolism' journal reported.
"Before our discovery, the mechanism behind how exactly the insulin-producing beta cells in the islet of Langerhans of the pancreas fail in type 2 diabetes was incompletely understood, making it difficult to design new and better therapies. Our research cracks open a decades-long mystery," said lead researcher Mehboob Hussain.
After a meal, the pancreas produces insulin to move glucose from the blood into cells for fuel. People with type 2 diabetes either don't secrete enough insulin or their cells are resistant to its effects.
In their study designed to figure out more precisely how the pancreas releases insulin, the team looked at how other cells in the body release chemicals.
One particular protein, Snapin, found in nerve cells, caught their eye because it's used by nerve cells to release chemicals necessary for cell communication. Snapin also is found in the insulin-secreting pancreatic beta cells.
To test the role of Snapin, the researchers engineered a change to the Snapin gene in mice to keep Snapin permanently "on" in the pancreas. They removed the pancreas cells and grew them in a dish for a day, then added glucose to the cells and took samples to measure how much insulin was released.
When the scientists compared that measurement to what was released by pancreas cells in normal mice, they found that normal mice released about 2.8 billionths of a gram of insulin per cell, whereas the cells from "Snapin-on" mice released 7.3 billionths of a gram of insulin per cell -- about three times the normal amount.
"We were surprised to find that the Snapin-on mice didn't have more or bigger pancreas cells, they just made more insulin naturally. This means all our insulin-secreting cells have this amazing reserve of insulin that we didn't really know existed and a switch that controls it," Hussain said.