Novel treatments, continuous innovation of healthcare technologies and a virtual limitless food and drink supply in the Western World have improved quality of life for many and resulted in an increase of life expectancy over the few past decades. However, just as we thought we solved the riddle of living longer and healthier, we have started experiencing the repercussions of unlimited food and increased convenience.

People are living longer, but not necessarily healthier. Our modern lifestyles of sedentary abundance are now challenging our health in new ways. Chronic diseases such as diabetes and obesity have seen an exponential increase and reached pandemic numbers.

At first glance, and a recommendation told to every type 2 diabetes patient many times during their treatment journey, it may seem as simple as a change in lifestyle could resolve the diabetes threat.  However, as billions of dollars in lifestyle education materials and programs show, it isn’t as simple as an extra walk around the block with the dog or a few less forkfuls of chocolate cake.

This week a new study published in Nature Medicine shows the results of one such research effort. I am one of the lead authors on the study which opens the path to potential new pharmacological strategies for the treatment of diabetes.

What are the findings?

The new study takes a closer look at the cells that produce insulin in the pancreas. Firstly, we aimed to identify novel drug-able markers that differ between diabetic and non-diabetic cells. Secondly, we tested whether there are additional mechanisms that contribute to the death of these cells, which ultimately leads to a lack of insulin, a hallmark of diabetes.

The results of our study identify a specific marker, known as the miR-200 family.  This marker is found in increased amounts in the insulin-producing cells in diabetes patients. We show this increase of miR-200 is functionally important and causally linked to pancreatic cell death. In fact, artificially increased levels of miR-200 induce pancreatic cell death, thus lowering the number of cells available to produce insulin and leading to the development of diabetes.

We have also found, in addition to the potential pharmacological relevance, reducing the amount of miR-200 can improve diabetes. This is due to the protective effect of miR-200 reduction, shifting the balance between cell survival and cell death in the favour of cell survival. As a consequence, the number of insulin-producing cells is increased and the body can better control blood sugar levels.

This means that if we can create a drug to block the miR-200 pathway in the insulin producing cells, then we may be able to slow or reverse the impact of diabetes (along with those often touted lifestyle changes).

What’s next?

Innovation of diabetes treatments has been slow over the past years compared to other disease areas. Studies like this one are of critical importance and may lead the way towards new drug targets. It remains to be seen whether all of them fulfil their promise, but it is an important step in the right direction.

Ultimately we will be only be able to cure diabetes if we combine the power of communication and science, thereby educating on a healthy lifestyle as well as providing state of the art treatment options.



Belgardt B-F*, Ahmed K*, Spranger M* et al. The microRNA-200 family regulates pancreatic beta cell survival in type 2 diabetes. Nature Medicine, advanced online publication, 18. Mai 2015. DOI: 10.1038/nm.3862


Diabetes, both type 1 & type 2, is characterised by elevated blood sugar levels and a failure of the body to control these. In the case of type 1 diabetes, this is due to a lack of the hormone insulin; whereas, in type 2 diabetes, the body has become resistant to the effects of insulin. At the centre of blood sugar regulation is one critical hormone, insulin, which is produced in the pancreas and upon food intake is secreted into the blood stream instructing the tissues and organs such as muscle, fat and liver to remove the sugar from the blood stream. If this process is impaired, a metabolic imbalance results, which, when uncontrolled, leads to co-morbidities such as kidney and nerve damage, eye disease as well as cardiovascular disease.