Type 1 diabetes is an autoimmune disease that occurs when certain cells of the immune system go awry and mistakenly recognize and kill (or inactivate) the insulin-producing β-cells. The β-cells are housed within the islets of Langheran along with the α-cells producing glucagon and other cells (footnote i). β-cells depletion leads to physiologically insufficient production of insulin and persistent high blood glucose. The disease is manageable with daily insulin injections and a healthy life style, but not curable. A cure would require the regeneration of the insulin-producing β-cells and the reeducation of the patient’s faulty immune system and significant progress is being made. Two research groups, one in Austria led by Dr. Stefan Kubicek
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Insulin is produced by the β-cells housed within the islets of Langheran (footnote i) of the pancreas. However, in people with T1D the β-cells are mistakenly recognized and killed, or disabled, by certain white blood cells (Leukocytes, footnote ii) of the immune system that has gone awry. Without the production of physiologically sufficient insulin the body’s glucose raises to life-threatening levels. Daily injections of insulin and a strict life style are the standard treatment of T1D, but it is difficult and annoying to closely adhere to them; and a poor compliance brings the risk of serious health complications. At the present, the only ways to stay off insulin are a total pancreas transplant (a very demanding surgery), or islets transplant (a relatively mild procedure), but these clinical procedures are limited to a few thousand patients because of shortage of pancreas donors and also have numerous shortcomings (described in Type 1 Diabetes Research Advances To Develop A Cure, part …show more content…
After a 4-day treatment of the β-cell depleted Zebrafish they found that the β cells of this animal model increased by about 75% compared to non treated animals. Also glucose levels in β-cell depleted zebrafish increased by 34% over normal zebrafish. However, upon artemether treatment Zebrafish had 42% lower glucose levels compared to normal animals. Moreover, in β-cell depleted rats a 23 days artemether treatment also resulted in a drastic reduction of blood glucose levels compared to non-treated animals.
Having shown success in animal models these scientists focused on intact human islets (apparently from donors without T1D). Artemether treatment of human islets in vitro (in Petri dishes) resulted in the reduced expression of α cell transcription factor ARX and increased insulin content compared to the untreated islets from the same donor. Moreover, in the presence of high glucose concentrations, significant more insulin was secreted by artemether-treated islets than from those
Insulin is produced by the β-cells housed within the islets of Langheran (footnote i) of the pancreas. However, in people with T1D the β-cells are mistakenly recognized and killed, or disabled, by certain white blood cells (Leukocytes, footnote ii) of the immune system that has gone awry. Without the production of physiologically sufficient insulin the body’s glucose raises to life-threatening levels. Daily injections of insulin and a strict life style are the standard treatment of T1D, but it is difficult and annoying to closely adhere to them; and a poor compliance brings the risk of serious health complications. At the present, the only ways to stay off insulin are a total pancreas transplant (a very demanding surgery), or islets transplant (a relatively mild procedure), but these clinical procedures are limited to a few thousand patients because of shortage of pancreas donors and also have numerous shortcomings (described in Type 1 Diabetes Research Advances To Develop A Cure, part …show more content…
After a 4-day treatment of the β-cell depleted Zebrafish they found that the β cells of this animal model increased by about 75% compared to non treated animals. Also glucose levels in β-cell depleted zebrafish increased by 34% over normal zebrafish. However, upon artemether treatment Zebrafish had 42% lower glucose levels compared to normal animals. Moreover, in β-cell depleted rats a 23 days artemether treatment also resulted in a drastic reduction of blood glucose levels compared to non-treated animals.
Having shown success in animal models these scientists focused on intact human islets (apparently from donors without T1D). Artemether treatment of human islets in vitro (in Petri dishes) resulted in the reduced expression of α cell transcription factor ARX and increased insulin content compared to the untreated islets from the same donor. Moreover, in the presence of high glucose concentrations, significant more insulin was secreted by artemether-treated islets than from those