Rise Of A Possible New Treatment For Diabetes: Smart Artificial β Cells
Since long, frequent and painful mechanical insulin pump or insulin injections for insulin infusion is used as a means for the treatment of type 1 diabetes and few cases of type 2 diabetes. However, a research team from the University of North Carolina has now designed what can be a much more patient-friendly alternative: artificial cells that release insulin automatically into the bloodstream when the levels of glucose increase.
These “artificial β cells” (AβCs) imitate the functions of the natural glucose regulators of the body, the pancreas’ insulin-secreting β cells. The dysfunction or loss of these cells results in type 1 diabetes and several incidents of type 2 diabetes. The notion is that the AβCs can be inserted subcutaneously into patients that would be substituted every few days, or by a disposable and painless skin patch.
Until now, insulin delivered in the form of a pill has been challenging, as it is a huge molecule that can be wiped out by digestive acids and enzymes prior to reaching the bloodstream. The main issue with existing insulin therapies is not that they cannot be carried in a pill, but that they cannot manage levels of blood glucose efficiently and automatically, the way normal insulin-secreting pancreatic cells do. In few cases, pancreatic cell transplants can resolve that issue.
Nevertheless, such cell transplants are costly, require donor cells that are mostly in short supply, need immune-suppressing drugs, and frequently fail owing to the damage of the transplanted cells. The research team has been exploring ways out to the insulin-delivery issue for much of the last decade. Thus, in this study, they implemented a predominantly ambitious strategy: creating artificial cells that, to a huge level, do what natural pancreatic β cells do.
AβCs, in this study, are produced with a simplified version of a 2-layered lipid membrane of a normal cell. The main advancement is what these cells enclose—specifically developed insulin-stuffed vesicles. A surge in levels of blood glucose directs to chemical alterations in the vesicle coating, resulting in the vesicles to initiate fusing with the outer membrane of the AβC, thereby discharging the insulin payloads.
The AβCs demonstrated a quick responsiveness to surplus glucose levels in diabetic mice w/o β cells and in lab-dish experiments. Gu said, “The mice went to normoglycemic from hyperglycemic within an hour, and stayed normoglycemic for about 5 Days after that.”
Gu and team are further planning preclinical tests and look forward to develop a means for transporting the cells painlessly through a skin patch that can be simply changed.