Diabetes is a disease associated with high blood sugar levels. Sugar (or glucose) is blocked from proper use in the body because the pancreas does not release insulin or the body can't use its own insulin as well as it should. In addition, the liver, which also is responsible for storing and making glucose, plays an important role in the maintenance of sugar levels.

In the development of diabetes disease contribute many factors such as: genetic factors, metabolic factors, immune system failure, infections, other organs dysfunction etc. But among thus the least studied is the role of brain. Brain seems to have a role into the pathology of many diseases, as recently scientist discovered a mysterious link between nervous system and immunity that was unknown piece of puzzle into relation of brain with immune system. Immune failure is a base for almost every disease directly or indirectly.

All of us know that diabetes harms our brain, but without permission of brain, a disease of diabetes mellitus cannot develop, recent studies showed this.

In the latest online issue of Nature, researchers from the Universities of Washington, Cincinnati and Michigan in the US, and the Technical University of Munich in Germany, present evidence of a brain-centered system that can lower blood sugar or glucose via insulin and non-insulin mechanisms.

They propose that normal glucose regulation relies on "highly coordinated interactions" between this brain system and the insulin-producing islets in the pancreas.

Should their suggestion be correct, it could open the door to completely new approaches to prevent and treat type 2 diabetes, perhaps even to reverse it, say the researchers.

Type 2 diabetes develops when the body does not produce enough insulin or the body's cells do not react to insulin (known as insulin resistance), with the result that blood sugar levels become too high (hyperglycemia).

However, the researchers say that this new research brings back the idea that the brain is involved – it suggests that normal glucose regulation depends on a partnership between the insulin-producing cells (the islet cells) of the pancreas and key circuits in the hypothalamus and other brain areas.

The authors argue that type 2 diabetes is the result of failure of both the pancreatic islet cell system and this brain-centered system for regulating blood sugar levels.

They review animal and human studies that document how the brain-centered regulatory system has a powerful effect on blood sugar levels independent of insulin.

One brain-centered mechanism uses a process called "glucose effectiveness" to promote glucose uptake in tissues. As this process accounts for nearly half of normal glucose uptake, it is on par with the insulin-dependent processes of the pancreatic islet cells.

The researchers propose a two-system model – the pancreatic islet system reacts to rising blood glucose by releasing insulin, and the brain-centered system enhances insulin-dependent glucose metabolism while also stimulating glucose effectiveness independently of insulin.

They say type 2 diabetes appears to be the result of failure of both systems.

According to the research, the brain system is the one most likely to fail first. This puts pressure on the islet system, which can compensate and carry on for a while, but then also fails, causing further decompensation in the brain system. The result is a vicious cycle of deterioration that ends in type 2 diabetes.

Introducing insulin reduces blood sugar back to normal levels but is only half the problem, say the researchers. You also need to tackle the brain-centered system failure. It may be possible not only to keep blood glucose under control, but also to cause a reversal of the type 2 diabetes, they write.


  • http://medicalxpress.com/news/2015-04-unraveling-link-diabetes-brain.html,
  • http://www.washington.edu/news/2013/11/06/brain-may-play-key-role-in-blood-sugar-metabolism-and-diabetes-development/,
  • https://www.sheffield.ac.uk/news/nr/impact-of-diabetes-on-the-brain-1.368336,
  • http://www.sciencedaily.com/releases/2013/11/131106141306.htm.