diabetes treatment

Scientists report breakthrough in finding new way to treat diabetes via cells in the pancreas

by Barbara Hewitt on July 31, 2018

A new potential way of treating diabetes has been discovered by scientists working on finding out more about how beta cells work in regulating blood glucose levels.

They have revealed that one of the building blocks in the calcium channels of beta cells in the pancreas could be used to treat the condition.

(dolgachov/Bigstock.com)

Beta cells in the pancreas produce the hormone insulin which regulates blood glucose levels and in people with diabetes these cells have lost part or all of their function.

The study by researchers at the Karolinska Institutet in Sweden explains that 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, triggering the release of insulin.

Under normal conditions the Ca2+ signal displays a specific regular pattern when the cells are stimulated by glucose. When, on the other hand, the beta cells are not able to release normal amounts of insulin, as in diabetes, this pattern changes.

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. The researchers have already shown that one of the building blocks in the channel, the so-called ß3 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 ß3 subunit and that this causes an altered Ca2+ pattern, a reduced release of insulin, and thereby impaired blood glucose regulation,’ said study leader Per-Olof Berggren, professor at the Rolf Luft Research Centre for Diabetes and Endocrinology at the Department of Molecular Medicine and Surgery at the university.

When the researchers reduced the amount of the ß3 subunit in the beta cells in the diabetic mice, the Ca2+ signal normalised and thereby the release of insulin, resulting in better regulation of the blood glucose levels.

The scientists also saw that mice that totally lacked the ß3 subunit demonstrated a better beta cell function and blood glucose regulation when they were given a diabetogenic diet. When the researchers tried transplanting beta cells without the ß3 subunit into mice with diabetes, the blood glucose regulation of the mice improved.

Experiments with human beta cells showed that the release of insulin deteriorates with increased amounts of the ß3 subunit.

‘Our findings indicate that just this building block in the calcium channel can be a new target for treating diabetes,’ said Berggren.

He added that even in type 1 diabetes manipulation of the beta 3 subunit may be beneficial in order to establish better functioning insulin secreting beta cells for transplantation.

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