Researchers suggest that targeting building block can combat diabetes, as per article published in the scientific journal Cell Reports in July 2018
Pancreatic beta cells produce hormone insulin for regulation of blood glucose level. In diabetic condition, beta cells loose part or all of their function. Calcium ions (Ca2+) act as an important signal for the release of insulin. When blood glucose increases, this causes the levels of Ca2+ in the beta cells to increase, accelerating the release of insulin. Under normal conditions the Ca2+ signal displays a specific regular pattern when the cells are stimulated by glucose. However, the beta cells are not able to release normal amounts of insulin, as in diabetes, this pattern changes. Researchers at Karolinska Institutet discovered that one of the building blocks in the calcium channels in the pancreatic beta cells play an important role in regulating our blood glucose values.
The level of Ca2+ increases in the beta cell when a specific calcium channel, made up of several different building blocks, opens in the beta cell’s wall. Per-Olof Berggren’s research group at Karolinska Institutet has previously shown that one of the building blocks in the channel, the so-called β3 subunit, plays an important regulatory role. “In our new study, we are able to show that beta cells from diabetic mice have an increased amount of the β3 subunit and that this causes an altered Ca2+ pattern, a reduced release of insulin, and thereby impaired blood glucose regulation,” said Per-Olof Berggren, Professor at the Rolf Luft Research Centre for Diabetes and Endocrinology at the Department of Molecular Medicine and Surgery at Karolinska Institutet.
For better regulation of blood glucose level, researchers reduced the amount of the β3 subunit in the beta cells in the diabetic mice, the Ca2+ signal normalized, which regulated release of insulin. Furthermore, it was observed that mice lacking the β3 subunit demonstrated a better beta cell function and blood glucose regulation when were administrated with diabetogenic diet. Furthermore, experiments with human beta cells reported low release of insulin with increased amounts of the β3 subunit.