New research from Columbia University suggests that intestinal cells can be manipulated into producing insulin. This would mean there is no requirement for a stem cell implant to achieve the same effect – recently researchers have agreed that stem cell implants would be the way forward for diabetes treatment.
Diabetes Type 1, or Diabetes Mellitus, is an illness characterized by the inability to produce insulin. This happens due to an autoimmune disorder that causes the destruction of Insulin producing cells in the Islets of Langerhans of the pancreas. The cells that produce insulin are specifically known as beta cells. The pancreas is incapable of recreating these cells and as a result there is diminshed (or non-existent) insulin secretion. This causes various elevated blood parameters, such as: elevated free fatty acids, elevated blood glucose, elevated blood ketone bodies etc.
As a result patients must frequently inject insulin and monitor their blood glucose using
glucometers, as glucose that is too high (hyperglycemia) or too low (hypoglycemia) are both dangerous conditions with the latter being extremely dangerous.
This new research comes as a ray of hope. The long term goal of diabetes research has been to find a way to replace these lost beta cells and research and theories pointed towards the use of stem cell implantation. This would remove the need for insulin injections as the cells would be able to self regulate themselves (via negative feedback and other stimuli) and insulin secretion would be physiological.
The current issue with using embryonic stem cell implants is that, while the cells can be manipulated to produce insulin, they do not release it in response to glucose. As a result they may release it at a time when it is not needed which could lead to hypoglycemia and could possibly be fatal.
The researchers found that a specific type of progenitor cell in the intestines of mice was capable of producing insulin when manipulated. Usually these cells would differentiate into cells that produce various gastric juices, serotonin, other GI hormones and gastric inhibitory peptide. However, by deactivating a gene known as Foxo1 – a well known decider of cell fate – the progenitor cells produced insulin secreting cells.
When Foxo1 was deactivated early on in development, it caused an increase in the number of progenitor cells that could secret insulin compared to deactivation at a later stage. However, insulin secreting cells were produced when Foxo1 was inactivated in adulthood.
The insulin produced from the gut cells worked as effectively as insulin produced by the pancreas or given via injection. The insulin secreting cells were also sensitive to changes in blood glucose – the fact that they have chemoreceptors (for glucose) makes them far safer and more reliable than the embryonic stem cells.
Research is now going to continue into developing or finding a drug that can deactivate Foxo1 in those intestinal progenitor cells and thus induce the production of insulin secreting cells.
Could this be the cure for Diabetes type 1 that people have been waiting for?