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Our bodies may cure themselves of diabetes in the future

Date:
January 4, 2019
Source:
The University of Bergen
Summary:
Diabetes is caused by damaged or non-existing insulin cells inability to produce insulin, a hormone that is necessary in regulating blood sugar levels. Many diabetes patients take insulin supplements to regulate these levels.
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Diabetes is caused by damaged or non-existing insulin cells inability to produce insulin, a hormone that is necessary in regulating blood sugar levels. Many diabetes patients take insulin supplements to regulate these levels.

In collaboration with other international researchers, researchers at the University of Bergen have, discovered that glucagon.producing cells in the pancreas, can change identity and adapt so that they do the job for their neighbouring damaged or missing insulin cells.

"We are possibly facing the start of a totally new form of treatment for diabetes, where the body can produce its own insulin, with some start-up help," says Researcher Luiza Ghila at the Raeder Research Lab, Department of Clinical Science, University of Bergen (UiB).

Cells can change identity

The researchers discovered that only about 2 per cent the neighbouring cells in the pancreas could change identity. However, event that amount makes the researchers are optimistic about potential new treatment approaches.

For the first time in history, researchers were able to describe the mechanisms behind the process of cell identity. It turns out that this is not at passive process, but is a result of signals from the surrounding cells. In the study, researchers were able to increase the number of insulin producing cells to 5 per cent, by using a drug that influenced the inter-cell signalling process. Thus far, the results have only been shown in animal models.

"If we gain more knowledge about the mechanisms behind this cell flexibility, then we could possibly be able to control the process and change more cells' identities so that more insulin can be produced, " Ghila explains.

Possible new treatment against cell death

According to the researchers, the new discoveries is not only good news for diabetes treatment.

"The cells´ ability to change identity and function, may be a decisive discovery in treating other diseases caused by cell death, such as Alzheimer´s disease and cellular damage due to heart attacks," says Luiza Ghila.

Facts: Pancreas

  • There are three different types of cells in the pancreas: alpha-cells, beta-cells and delta-cells. These produce different kinds of hormones for blood sugar regulation.
  • The cells make clusters. Alpha-cells produce glucagon, which increases the blood sugar levels. Beta-cells produce insulin, which decreases glucagon levels. Delta-cells produce somatostatin, which controls the regulation of the Alpha and Beta Cells.
  • Persons with diabetes have a damaged beta-cell function, and therefore have constant high blood sugar levels.

Story Source:

Materials provided by The University of Bergen. Note: Content may be edited for style and length.


Journal Reference:

  1. Valentina Cigliola, Luiza Ghila, Fabrizio Thorel, Léon van Gurp, Delphine Baronnier, Daniel Oropeza, Simone Gupta, Takeshi Miyatsuka, Hideaki Kaneto, Mark A. Magnuson, Anna B. Osipovich, Maike Sander, Christopher E. V. Wright, Melissa K. Thomas, Kenichiro Furuyama, Simona Chera, Pedro L. Herrera. Pancreatic islet-autonomous insulin and smoothened-mediated signalling modulate identity changes of glucagon α-cells. Nature Cell Biology, 2018; 20 (11): 1267 DOI: 10.1038/s41556-018-0216-y

Cite This Page:

The University of Bergen. "Our bodies may cure themselves of diabetes in the future." ScienceDaily. ScienceDaily, 4 January 2019. <www.sciencedaily.com/releases/2019/01/190104104020.htm>.
The University of Bergen. (2019, January 4). Our bodies may cure themselves of diabetes in the future. ScienceDaily. Retrieved March 28, 2024 from www.sciencedaily.com/releases/2019/01/190104104020.htm
The University of Bergen. "Our bodies may cure themselves of diabetes in the future." ScienceDaily. www.sciencedaily.com/releases/2019/01/190104104020.htm (accessed March 28, 2024).

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