New Hope for Pancreatic Beta Cell Regeneration Cure for Diabetes

Further research into the vital beta cells in the pancreas that produce the hormone insulin have thrown up facts that could lead medical science a step closer to a cure for diabetes.  They have identified a protein that causes the beta cells to grow large and strong – and another enzyme that destroys this beneficial protein.

In type 1 diabetes, the beta cells in the Islets of Langerhans have been damaged or destroyed by an auto-immune reaction which is still not thoroughly understood.  The patient then becomes diabetic because his pancreas does not produce insulin, and he is diagnosed typically because he is manifesting symptoms.  These include increased thirst and hunger, increased production of urine, extreme fatigue, poor healing, and recovery from infection, weight loss, and cramps.

The patient, typically a young person aged 20 or younger, has then to become accustomed to a new lifestyle, with regular blood sugar testing and injections to control his blood sugar levels.  While the mortality of diabetics is higher than that of non-diabetics, he can still live a relatively normal life with a reasonable life expectancy if he takes care of himself and follows his healthcare regime.

Dr Marcus Stoffel, an award-winning professor atZurich’s Swiss Federal Institute of Technology, and his team previously discovered a protein they called Tmem27 on the surface membranes of the pancreatic beta cells.  As higher concentrations of Tmem27 were linked to increased growth of the islets of Langerhans, site of the beta cells, in mice, they concluded that this protein activated the growth.  They also found cleaving or fragmenting the protein made it inert.

Dr Stoffel, who received the Juvenile Diabetes Research Fund’s Gerold & Kayla Grodsky Basic Research Scientist Award, said the team theorized that if they could prevent the protein from being cleaved and increase its levels it could increase beta cell growth and thus insulin production.  They therefore investigated what was causing the cleaving of Tmem27, and found an enzyme protein called Bace2 also found on the surface membranes of the beta cells.  They discovered that lower levels of this enzyme were linked with larger islets of Langerhans and more beta cells both existing and being generated in the laboratory mice.  Mice with less Bace2 were also better at lowering their blood sugar than mice with higher levels of the protein.

The team then experimented with lowering the Bace2 levels of the mice, and found giving them a compound that inhibited Bace2 caused their beta cells to start regenerating.  The researchers also found an enzyme called Bace1, which is chemically similar to Bace2, does not cleave the Tmem27 protein.  Although Bace1 is associated with other health conditions such as Down’s Syndrome and Alzheimer’s, it can still be studied as part of research to develop a Bace2 inhibitor and find a therapy for diabetes based on these discoveries.  The team hopes that this investigative route could lead to the development of therapies to boost beta cell regeneration and produce a cure for type 1 diabetes.  The research may also lead to better and quicker diagnosis of diabetes through measuring the amounts of cleaved Tmem27 in the bloodstream, which would indicate levels of Bace2.

Next Post → ← Previous Post