I try to write about different clinical topics as well as pertinent research in pediatric diabetes. Stem cells are a very hot topic in many areas of biology! Researchers are coaxing stem cells from organs other than the bone marrow (or from embryos) that are demonstrating amazing possibilities. One of the most exciting concepts that I recently noted was that despite having long-standing diabetes, the pancreas still had evidence of living beta cells as evidenced in the “Joslin Gold Medal” study of people with diabetes that died from natural causes. The dogma that we are born with only a certain number of cells in specific organs is starting to unravel.
A recent publication in PLoS "Adult Pancreas Side Population Cells Expand after β Cell Injury and Are a Source of Insulin-Secreting Cells"; Banakh I, Gonez LJ, Sutherland RM, Naselli G, Harrison LC; PLoS ONE 7(11): e48977, published online 9 Nov 2012; DOI:10.1371/journal.pone.0048977 has excited many researchers in the type 1 diabetes community. This study is a basic science research study that hopefully will move from “bench” to practice rapidly (translational medicine).
Drs. Ilia Banakh, Len Harrison, et al., from Australia’s Walter and Elizabeth Hall Institute’s Division of Molecular Medicine published how they identified and isolated stem cells from the adult pancreas. After this process, they were able to force them into cells that could manufacture insulin when exposed to glucose! According to the authors, “the side population of cells in the adult pancreas expand in response to Beta cell injury and are a source of B Cell progenitors with the potential for the treatment of diabetes.”
What are side populations of stem cells?
By definition (based on DNA binding dyes and ATP-binding cassette transporters), the side population of cells in adult tissues has stem cell properties. The authors hypothesized that the side population of cells would expand “in response to B cell injury and produce functional Beta cells.” The side population cell numbers increased significantly in response to partial pancreatectomy in the absence of high blood sugar. The side population of cells thus proliferated and changed into beta cell islet cells that actually produced insulin in response to glucose. The insulin expression continued for at least 2 weeks when tissue was transplanted within “vascularized” chambers into mice with diabetes.
Why is this research significant?
It is becoming clear that stem cells are not only present in embryos, but also may be able to proliferate from other organs, such as the pancreas. It might be possible someday for humans to be able to regenerate insulin-producing cells that may be similar or identical to beta islet cells. However, this is only part of the problem in autoimmune type 1 diabetes. For the beta cells to survive and continue to produce insulin, the autoimmune response must be eliminated or at least, attenuated. However, if one can protect the islet cells after they have been coaxed to proliferate by some sort of capsule or membrane that may prevent killer cells from attacking, we could perhaps “cure” type 1 diabetes.” It appears that we may be able to supply fresh insulin-producing beta cells, but will need some way to protect them if we cannot prevent the immune response.