Scientists at the Swiss Federal Institute of Technology have found a link between a protein called beta secretase-2 (Bace2) and diabetes type 1 which is characterized by the autoimmune destruction of beta cells in the pancreas that are responsible for the production of insulin. There is another protein player at work here called Tmem27. Both beta secretase-2 and Tmem27 are glycoproteins that are found outside the pancreatic beta cell walls.
The scientific team’s research led to an ominous observation; the removal of Tmem27 from the cell’s external wall brings death to its corresponding beta cell. More importantly, their research suggested that beta secretase-2 is responsible for the destruction of Tmem27. However, if we could somehow medically induce heightened production of pancreatic beta cells, this would break major ground in the way we view and treat diabetes today.
As it turns out, this is exactly what those researchers are attempting to do. In fact, they were able to produce a chemical that inhibits the activity of beta secretase-2 in diabetic mice, therefore halting the destruction of Tmem27 and thusly increased the proliferation of pancreatic beta cells in mice. It was concluded that diabetes in these mice receded. With healthy beta cells, diabetes type 1 patients would no longer need to worry about their low insulin levels.
The results of this scientific study has allowed others to join in on the pursuit of developing a therapeutic drug for humans that targets and inhibits beta secretase-2 without allowing it to pass through the blood-brain barrier. As of right now however, trials for the drug are only commencing development by companies like Novartis, Roche, Jortan Pharmaceuticals and Schering AG.
Diabetes is a worldwide epidemic that has been on the rise for decades now. With a potential new drug, generically known as beta secretase inhibitor II entering the market, we might be able to say that a cure for diabetes is at our doorstep and that continuing research and development to perfect its targeted action would most likely lead to a major chemically therapeutic breakthrough for diabetic patients. We would no longer hear about diabetic patients becoming “insulin-dependent” since beta cell proliferation would normalize insulin-associated metabolic processes that have gone awry along the way; exactly what the doctor ordered.