Drug Clears Unhealthy Insulin-Producing Cells, Preventing Early Diabetes in Mice was reported by Nicholas Weiler on UCSF News, 21 February 2019. A UC San Francisco study of human and mouse pancreatic tissue suggests a new origin story for type 1 (T1) diabetes. The findings flip current assumptions about the causes of the disease on their head and demonstrate a promising new preventative strategy that dramatically reduced disease risk in laboratory animals.
In a study published Feb. 21, 2019, in Cell Metabolism, UCSF Diabetes Center professor Anil Bhushan, PhD, and his team show that pancreatic beta cells themselves may play a much more active role in T1 diabetes than previously appreciated, opening the door to a totally new avenue for therapy.
Bhushan, who has long studied the biology of pancreatic beta cells, said that he has never been completely satisfied with the dominant model of the origins of type 1 diabetes. The researchers found that well before immune cells began to attack the pancreatic islets where beta cells reside, the beta cells began exhibiting signs of “secretory senescence,” a type of cellular decline caused by DNA damage in which cells stop functioning properly and begin producing molecules that harm nearby cells and attract the attention of the immune system.
“Perhaps therapies should find a way to do the job the immune system is failing to do: clear the senescent cells early on,” Bhushan commented.EXCITING RESEARCH!
To test whether eliminating senescent beta cells could help prevent T1 diabetes, Bhushan’s group tested a drug, recently approved by the FDA as a chemotherapy agent for a type of leukemia that also acts as a so-called senolytic — a drug that selectively eradicates senescent cells.
Remarkably, the researchers found that while 75 percent of control mice developed diabetes by 28 weeks of age, only 30 percent of mice who were given the drug for two weeks prior to the onset of symptoms went on to develop the disease. The researchers showed that the drug had rapidly eliminated senescent beta cells in these mice, after which their immune systems (which were not directly affected by the treatment) left the remaining, healthy beta cells alone, avoiding the loss of insulin production that causes diabetes.
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Oxygen Critical to Practical Islet Transplants was reported by Martin Hensel of InsulinNation.com, 2 April 2019. For islets to survive the body’s immune system, the implanted islets need to be isolated from any direct contact with any cells from the recipient, including all white and red blood cells. At the same time, islets need oxygen to function.
Klearchos Papas, PhD (professor in the Departments of Surgery, Medical Imaging, and the BIO5 Institute at the University of Arizona College of Medicine – Tucson) in collaboration with the Center for Magnetic Resonance Research at the University of Minnesota, is developing an oxygen generator-based islet ‘tea bag’ transplant device for which the JDRF just funded a pre-clinical study.
“We call it a tea bag because it consists of two side-by-side layers of islets that are enriched with oxygen. It is a tiny device which when implanted under the skin senses glucose levels and releases insulin when needed.” The subcutaneous location of the tea bag makes installation and replacement a simple office procedure. The life expectancy of the islets and the tea bag is expected to be between 1-3 years but theoretically, it could last a lot longer, even up to 10-15 years. It is conceivable that a booster of islets could be installed in an already-implanted tea bag.
During initial clinical trials, a wearable oxygen generator is anticipated. Development of an implantable generator does not require new science but it will be expensive to miniaturize the device and enable recharging of its batteries outside the skin via some field effect approach similar to modern phone chargers.