Scientists discover potential new targets for treating type 2 diabetes

Medical Network August 3rd Researcher from the Karolinska Institute published in an article in the international journal Cell Reports found that a module in the calcium channel of islet beta cells plays an important role in regulating our blood sugar. Treatment for this module will likely become a new approach to fight type 2 diabetes.

The beta cells in the pancreas are responsible for the insulin that regulates blood sugar in our body. In diabetes, beta cells lose some or all of their function. Calcium ions are an important signal in the release of insulin. An increase in blood glucose leads to an increase in the concentration of calcium ions in the beta cells, which causes the release of insulin. Under normal conditions, the calcium signal will show a specific mode of regulation when the cells are stimulated by glucose. On the other hand, when beta cells are unable to release normal amounts of insulin, such as in diabetes, this pattern changes.

Identify the cause of reduced insulin release

When a particular calcium channel composed of several different modules is opened in beta cells, the level of calcium ions in the beta cells increases. The research team at Karolinska Institute has previously shown that a module called the β3 subfamily in the calcium channel has important regulatory effects.

"In our new study, we can clarify that the number of β3 subfamilies in beta cells of diabetic mice has increased, which has led to changes in calcium regulation patterns, reduced insulin secretion, and thus impaired glycemic regulation," Leader, Berggren, professor of the Rolf Luft Center for Diabetes and Endocrinology at the Karolinska Institute of Molecular Medicine and Surgery, said.

Better regulation of blood sugar levels

When the researchers reduced the number of β3 subfamilies in the beta cells of diabetic mice, the calcium ion signal became normal and thus normalized insulin secretion, thereby better regulating blood glucose levels. They also observed that mice that were completely deficient in the β3 subfamily showed better beta cell function and blood glucose regulation when given a diabetes-producing diet . When researchers attempted to transplant beta cells that did not contain the β3 subfamily into diabetic mice, their blood glucose regulation ability was restored.

Human beta cell assays have shown that insulin secretion is attenuated as the number of β3 subfamilies increases.

"Our findings suggest that this module of calcium channels can be a new target for the treatment of type 2 diabetes. However, even manipulation of the beta 3 subfamily in type 1 diabetes is beneficial for establishing better insulin function." Berggren said.

Original source: Kayoung Lee et al. Blocking Ca 2+ Channel β 3 Subunit Reverses Diabetes, Cell Reports (2018). DOI: 10.1016/j.celrep.2018.06.086