London: Scientists have created a new technique to procude cells with insulin-secretion capabilities that may be transplanted in patients with Type 1 diabetes in the near future.
Currently one of the most promising therapies in the fight against diabetes is the replacement of beta cells in pancreas.
In the replacement therapy for Type 1 diabetes, researchers from Université Catholique de Louvain (UCL) in Belgium have previously shown that human pancreatic duct-derived cells (HDDCs) are an attractive source of cells.
The cells are found in the adult pancreas and are progenitor cells – cells that have a tendency to differentiate into specific types of cells.
In the new study, the group reprogrammed HDDCs to behave like beta cells and secrete insulin within the pancreas, while responding to glucose.
The researchers used a specific protein that controls which genes are turned off or on in the genome. This technique allowed them to avoid any potential genetic modification of the target cells.
“The novelty of our work resides in the use of adult tissue that avoids the risks related to stem cells, such as cancer, and of a protocol that modifies the cells with a direct action on DNA without any structural modification,” explained lead investigator professor Philippe Lysy.
“Our system for cellular reprogramming opens doors for experiments in other scientific fields with the objective to produce cells with a new function in the context of diseases with a loss-of-function,” he added.
The group has already developed a mouse model that allows them to transplant their manufactured cells into the diabetic mice and follow-up on their disease.
It is well established that in Type 1 diabetes, the body’s immune system mistakenly attacks and destroys beta cells in the pancreas.
These unique cells are responsible in producing, storing and secreting insulin – the hormone that regulates levels of glucose in the blood.
The findings were presented at the 54th annual European Society for Paediatric Endocrinology meeting in Spain on Thursday.