The drug otelixizumab appears to halt the rapid decline in the body’s production of insulin, according to a recent study published in the journal ‘Diabetologia’. This rapid decline of insulin production occurs in people with Type 1 diabetes due to an auto-immune response.
The drug works by switching off the immune system's self-destruct mechanism that causes Type 1 diabetes. This halts damage to the pancreas, allowing it to carry on producing insulin.
In a person without Type 1 diabetes the immune system protects the body against infection by releasing two types of cells. ‘T effector’ cells are released to attack the invading bacteria and viruses, while ‘T regulatory’ cells are dispatched to keep the ‘T effector’ cells in check and stop them from doing more harm than good.
One theory behind Type 1 diabetes is that this balance tilts too heavily in favour of the ‘T effector’ cells, so they not only attack invading organisms but healthy tissues and organs as well.
The new drug contains a very specific antibody that targets a marker found only in ‘T effector’ cells. Once the drug locks onto the cells, it stops them destroying the insulin-producing cells in the pancreas.
In the study patients given the six-day treatment continued to produce their own insulin, or needed to inject only small amounts. In contrast, a group given a placebo needed rapidly increasing amounts of injected insulin.
The results show that otelixizumab can either halt or dramatically reduce the need for insulin injections among people newly diagnosed with diabetes.
Research suggests the effects might wane after a couple of years, when further treatment would be required. But if it does prove successful in larger trials, it could be available in Britain within the next five years.
“We welcome this study as a positive step forward," said Dr Iain Frame, Director of Research at Diabetes UK.
“This is one of a number of similar approaches being undertaken to delay the onset of the condition, and we have been watching such developments with great interest.
“But the treatment appears to be dependent on the amount of residual insulin-producing cells left in the patient and their age at the time of the treatment.
“It's worth remembering that this approach will not be suitable for those who have had Type 1 diabetes for some time.”