Wouldn’t it be great to eliminate all that day-to-day pricking and pronging of what is called diabetes? Well it soon might be possible. Type 1 diabetes is the autoimmune disorder in which cells in the pancreas are destroyed. As these cells develop only during embryonic development, they cannot be replaced and thus insulin is not produced. However, researchers have just discovered that by deleting the gene Foxo1, insulin cells can be generated in the gut rather than in the pancreas. This could be a possible treatment for people with type 1 diabetes.
The process of induced insulin production begins in the intestinal tract. Within the stomach and intestines there are cells called Neurog3+ enteroendocrine progenitor cells, but we are just going to call them NEP cells for short. These cells are continuously produced by stem cells in the gut. They are also original or precursor cells that are able to differentiate into many other different cell types. This differentiation process is carried out as follows:
- Each NEP cell is a diploid cell with all of them containing the same genome (the entire hereditary information).
- These cells then differentiate into two new daughter cells. Each daughter cell ‘selects’ and expresses a distinct set of genes from their shared genome, resulting in different cell types.
Some of these new cell types are equivalent to those which are usually produced in the pancreas. However the gene Foxo1, located in the NEP cells, supresses the production of insulin positive (Ins+) cells. This means that only cells which lack or are deficient in the gene are able to produce insulin cells. Therefore by using a toxin to ‘knock out’ the gene Foxo1, Ins+ cells showing mature β cells are formed. Containing mature beta cells demonstrates that the Ins+ cells are also able to create and release insulin. These new cells are able to regenerate rapidly and are additionally glucose-responsive. Unlike embryonic stem cell treatment for diabetes, through this new process Ins+ cells release insulin in a glucose-regulated manner (when blood glucose levels increase). This property is believed by researchers to be due to the shared glucose-sensing receptors between normal pancreatic β and NEP cells. The ability to release insulin to control glucose levels is a key concept in the body, as high or low levels of glucose can have serious consequences. By removing the gene Foxo1 in Neurog3+ enteroendocrine progenitor cells, a treatment for type 1 diabetes could be found.
Therefore, Neurog3+ enteroendocrine progenitor cells, or NEP cells, in the intestinal tract can be induced into producing insulin positive cells. By removing the gene Foxo1 in these progenitor cells, Ins+ cells are independently formed which, in turn, release insulin in response to blood glucose levels in the body. This process may be the start of eliminating the day-to-day pricking and pronging of diabetes. It could be the breakthrough treatment required to restore insulin production in type 1 diabetics.