Sunday, 15 February 2015

Could diabetes become curable within the next 10 years?



Image retrieved from Scientific American
In Britain today, more than 29,000 people are diagnosed with either type 1 or type 2 diabetes. 1 in 3 adults suffer from diabetic-like symptoms, including fatigue, high blood sugar and problems with vision.
Diabetes is diagnosed in every 17 out of 100,000 children yearly in England and Wales. Although the least common type as a whole, 90-95% of diabetics under 16 have Type 1 diabetes, which is normally caused by genetic factors in an individual.
Because of this, hundreds of research projects around the world are dedicated to treating, preventing and possibly curing the condition that affects the daily lives of so many people.

But how close are we to actually “curing” diabetes in humans? What research is out there, and what changes can we expect to see in the next decade?

This article aims to illustrate some of the pioneering studies in several institutions that are tackling type 1 diabetes. Before this, here is an explanation of the disease and how it affects the body:

Type 1 Diabetes Mellitus is an autoimmune disease, which means that it causes the body to attack itself. Autoantibodies – immune system components that mistakenly break down tissue in the body – attack beta cells in the pancreas. These specialised cells secrete a hormone called insulin, which acts to lower glucose levels in the bloodstream after eating or during periods of rest. The damage to the beta cells means that they cannot secrete insulin, causing dangerously high concentrations of glucose in the blood to bring about symptoms such as hyperactivity, frequent urination and increased thirst.
When all of the glucose in the blood has been used up, the body goes into panic mode because there isn’t any stored glucose around for energy. This is called hypoglycaemia, and leads to symptoms such as blurred vision, extreme tiredness and in severe cases, epileptic seizures.
Diabetes can be treated by frequent administrations of insulin to keep blood-glucose levels at bay, although this can be inconvenient and enforces a diet that has to comply with the insulin doses. The insulin has to be administrated intravenously, either through a small pump-device attached to the body or by injections. No cure is available for diabetes at this moment.

The first study in this article looks at a 3 year analysis of 33 infants in Finland, who were selected for their genetically-higher risk of developing type 1 diabetes. The researchers wanted to look at the progress of each infant as they grew up. By the age of 3 most of the children were healthy, but 4 had already developed diabetes. When analysing these children, researchers discovered a significant absence of body flora in their gastrointestinal tracts (GIT). Body flora is the “good” bacteria found in an individual’s body, and can be found on the skin, in mucous, but mostly in the GIT.
When the body floras of the diabetic children were studied, larger than normal populations of species were found that trigger inflammation of the GIT - which has been known to be a secondary symptom of diabetes as the species are thought to also attack the beta cells in the pancreas.

When looking at the healthy children, 11 of them had already started to produce autoantibodies. The researchers wanted to know why the autoantibodies hadn’t caused the disease in these children, so they came up with the idea that normal, or enhanced, levels of body flora in the body were tackling the onset of the condition in the children.

To extend on this hypothesis, a study in New York shows the bacterium Lactobacillus gasseri (found in probiotic yoghurt) can transform intestinal cells in rats to act like beta cells and secrete insulin. The bacteria possess the enzyme Glucagon-peptide 1, which is thought to bring about the intestinal cell changes. The study observed diabetic rats being fed probiotic yoghurt for 30 days, and found that at the end of the observation the rat’s had a 30% drop in glucose levels compared to healthy rats. Moreover, the diabetic rats could use their insulin-secreting intestinal cells to reduce their blood sugar levels as fast as their healthy counterparts.
This study takes the hypothesis of positive body flora modification and applies it practically. The next step in application would be to produce a bacteria-containing pill that diabetics could take daily, instead of injections.

Probably the most notable breakthrough in diabetes this decade came from a Harvard diabetes institute in October 2014. After 23 years of research initiated by the diagnosis of his son with type 1 diabetes, Dr Doug Melton and his research group managed to produce artificial, insulin-secreting beta cells from stem cells. The “beta units” were observed to secrete the hormone upon glucose-induced stimulation, resemble typical beta cells found in the pancreas genetically and structurally, and in transplantation manage to bring about a positive effect on hyperglycaemic mice.
The stem cell-derived beta cells are currently undergoing trials in other animals, but not yet primates. Because of the complexity of artificial cells we may not see beta cell transplantation in humans for at least another decade.

 A final study that deserves attention is an ongoing project at the Massachusetts Institute of Technology (MIT).  Researchers are experimenting with insulin release mechanisms by modifying the hormone itself. So far, the team at MIT have been able to change the chemical structure of insulin molecules so that it stays in the blood stream for longer, which would mean for patients that frequent injections of the hormone would not be needed. The researchers have achieved this prolonged presence of insulin by adding a hydrophobic (water-repelling) domain to the molecule. The theory behind this is that the molecule would be more likely to bind to proteins in the blood, preventing it from being broken down by sugars.
Image retrieved from Medcity News
As well as adding the domain to the molecule, a chemical group was added that binds to glucose and brings it into contact with insulin. Therefore, in high concentrations of sugar, protein-bound insulin is likely to be broken down by surrounding glucose. The combination of these two mechanisms means that insulin can not only stay in the blood for longer periods of time, but also still reduce blood-glucose levels when the blood is hyperglycaemic.
This modified insulin has already been tested on mice that are deficient in the hormone. The results showed the mice reacting more efficiently to spikes in blood-glucose concentration, compared to traditional insulin.
At this moment, further test-stages are required before this treatment can be made available on any health service, but the project is ongoing and the researchers at MIT are dedicated to produce the modified hormone in purer and safer quantities.


The field of diabetic research is a constantly progressing, and has been at an immense speed since the 1990s. Molecular biology, pharmacology and the fairly recent advanced understanding of cell biology has made all of this possible. Just by looking at the 3 studies mentioned, it’s fair to say that diabetes will become a curable disease within the next 10 years. 







Images retreived from : http://medcitynews.com/2014/04/jdrf-partners-insulin-startup-thermalin-ultra-rapid-acting-insulin-t1d/

http://www.scientificamerican.com/article/a-diabetes-cliffhanger/