DRC & Research News

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Senescent Cells May Play Integral Role in Type 1 Diabetes

For years, the general consensus among scientists was that type 1 diabetes (T1D) was caused by the immune system erroneously destroying insulin-producing beta cells. Researchers have yet to determine exactly why the immune system reacts this way in some people but not others. A new study exploring cellular changes prior to the development of diabetes may have unlocked an important piece of the puzzle.

Research conducted by a team from the UCSF Diabetes Center has revealed that secretory senescence in some insulin-producing beta cells in the pancreas may be a trigger for this massive cellular destruction. When DNA damage causes cells to malfunction and harm surrounding cells, that is when the immune system kicks in and attacks the beta cells. But researchers have found this only occurs once the senescence has become widespread. If these senescent cells are eliminated early on, it may help prevent the onset of T1D because only damaged cells would be destroyed while healthy cells would remain.

The scientists studied both mouse models and pancreatic tissue from deceased human donors with diabetes. By administering an FDA-approved second-line chemotherapy agent called ABT-199 or Venetoclax, they were able to selectively target and destroy senescent beta cells in the pancreas. In their study, only 30 percent of mice given this drug developed T1D, while 75 percent of control mice developed T1D. Furthermore, the drug did not have any direct impact on healthy beta cells or the immune system in general.

Overall, they found that the risk of developing T1D could be decreased through the use of ABT-199. Further studies are necessary to determine whether periodic administration of the drug continues to clear senescent cells and keep the disease at bay. If so, this could become a potential new treatment option in the fight against T1D.

The Diabetes Research Connection (DRC) is interested in seeing how this discovery plays out and impacts future diabetes research and treatment. It could open doors to new treatment therapies and approaches for decreasing the risk of T1D through early intervention. The DRC supports early career scientists in accessing critical funds to support novel research studies focused on the prevention, treatment, and cure of T1D as well as improvements in quality of life for individuals living with the disease. To learn more, visit http://diabetesresearchconnection.org.


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Influencing Cell Development to Support Type 1 Diabetes Treatment

One of the strategies researchers have been exploring for treating Type 1 Diabetes (T1D) is getting the body to generate new insulin-producing islet cells, or keeping it from destroying implanted cells. In individuals with T1D, the body does not produce enough insulin on its own to manage blood sugar levels because the immune system attacks and destroys these islet cells.

In a recent study, scientists at the University of Copenhagen (Denmark) and the Helmholtz Zentrum München (Germany) may have found a way to influence cell development in order for the body to produce more insulin-producing cells on its own. This could play an integral role in the development of improved treatment options for T1D.

The scientists closely examined a type of immature cells in the pancreas known as progenitor cells. They are similar to stem cells in that they can develop into different types of mature cells, but the variety is more limited, and they cannot divide and reproduce indefinitely. Mainly they become either endocrine beta cells or duct cells. Endocrine cells include islet cells.

By carefully studying the constant movement of these progenitor cells, researchers found that their development is strongly impacted by their environment and what types of structures they interact with. When they have greater interaction with the extracellular matrix laminin, they are more likely to become islet cells. When there is greater interaction with fibronectin, this leads to increased mechanical forces within the cell, in turn increasing the likelihood of development into duct cells.

Scientists believe they can transition this understanding to the development of stem cells in order to generate more insulin-producing islet cells by taking advantage of the mechanosignaling pathway. In terms of treatment options, this could contribute to the advancement of cell replacement therapies.

It is encouraging to see how researchers are enhancing and evolving their understanding of how cellular processes are related to type 1 diabetes and how these findings can support improved treatment options. Though not involved with this study, the Diabetes Research Connection strives to further these types of efforts by providing critical funding to early career scientists pursing research on T1D.


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