Humans can recode human alpha and gamma islet cells to produce insulin. Normally, only the beta cells of the pancreas can produce insulin. After the modified cells were transplanted into diabetic mice, the diabetic symptoms of the mice were alleviated. After stimulation
The transformation of “post-cells” into different cell types is a widespread regeneration strategy in animals, but it is rarely documented in mammals. In mice, the destruction of insulin-secreting pancreatic β cells can cause the non-β cells of the pancreatic islets to produce insulin. It is not clear whether human islet cells can show the same plasticity. Pedro Herrera of the University of Geneva, Switzerland, and colleagues investigated whether human islet alpha and gamma cells from diabetic and non-diabetic donors can be recoded to produce an insulin response to glucose. The authors report that increasing the expression of two major transcription factors (Pdx1 and MafA) allows cells to produce insulin, which is the first direct indicator of the plasticity of mature human non-beta cells in the pancreatic islets. prove. in
After, the researchers tested whether these insulin-producing human α cells can alleviate the clinical manifestations of type 1 diabetic mice lacking pancreatic β cells. After transplanting insulin-producing α cells from multiple donors into mice, the mice's glucose tolerance, secretion and blood levels were standardized. After transplantation, the cells continue to secrete insulin for up to 6 months. These findings provide conceptual evidence for the plasticity of human islet cells. Nourishing this plasticity to replace the lost cell population may represent a potential treatment for diabetes and other degenerative diseases.