Could diabetes be considered an inflammatory disease?

Inflammation is a coordinated response by the cells of our immune system to damage to the body or to the presence of an infectious agent.

This can be located in an area of ​​the body and is characterized by pain, redness, heat, stiffness and swelling. Although it may seem like a bad sign of the body, inflammation is necessary to eliminate bacteria or viruses that cause infections.

However, there are times when the immune system attacks or destroys tissues in our body by mistake. In this way, it participates in the development of many types of diseases such as arthritis, Parkinson’s or diabetes.

Inflammation alerts us to possible damage

When some type of damage occurs in our body (a tissue injury caused by a fall or an infection), inflammasomes come into play. These are one of the components of our immune system responsible for producing inflammation when they detect damage or the presence of pathogens. That is, our cells have these inflammasomes so that it produces the necessary inflammation according to the damage produced.

Having these inflammasomes under control is very important because if they are always in operation they are harmful to our body because we can develop or worsen diseases. As an example of diseases associated with the lack of control of these inflammasomes we find autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, or neurodegenerative diseases such as Alzheimer’s, systemic sclerosis or Parkinson’s.

Today, inflammasomes are of medical interest as a possible target to alleviate or even cure various conditions. Therefore, it is important to know how they work in order to develop future drugs that alleviate different diseases, as they have recently done at the University of Murcia. But before knowing their findings, we will remember how this disease develops.

Why is diabetes produced?

When we eat, glucose from food reaches our blood. At this time, beta cells (pancreatic cells) produce insulin (a hormone) and insulin allows glucose to enter tissues, such as muscles or the brain. Thus it can be converted into energy.

If our pancreas cannot produce insulin or this insulin is defective, glucose in the blood cannot enter the tissues. Then it accumulates in the blood, which can be dangerous to health. We know this situation as diabetes.

It is a chronic autoimmune disease that affects a large number of people in the world. In fact, it was the direct cause of death of more than 1.5 million people in 2019 according to WHO.

Until now, diabetes has only been viewed as a metabolic disease. The origin of the inflammation had not been taken into account. But knowing it implies that we can develop new therapeutic tools to be able to treat these patients.

What does diabetes have to do with inflammation?

It has recently observed that inflammasomes are intervening in the development of diabetes.

Different studies have shown that people with diabetes have an activated beta-cell inflammasome.

In addition, in another work carried out in mice to which they had been eliminated the inflammasome genetically, they did not develop diabetes or they did it at a much lower level than those with inflammasome.

For all this, it is believed that the inflammasome releases proteins that activate inflammation, causing the destruction of these cells of the pancreas. As a consequence diabetes develops. Therefore, diabetes would have a preclinical phase linked to chronic inflammation.

Although we know the cellular mechanisms that could intervene in this process and which genes could be involved, the origin of this inflammation and the factors that trigger it could vary and are not yet fully known.

A vicious cycle of inflammation

But inflammation not only plays an important role in causing diabetes, but also in the problems derived from it. We know that a continuous increase in blood glucose over time above normal values ​​(such as 120 mg / dl) can cause inflammation.

In turn, this inflammation could cause significant damage to blood vessels and organs such as the kidneys or eyes. Although the mechanisms involved in this process are still in the study phase. Therefore, controlling this chronic inflammation is also essential for optimal treatment of patients with diabetes.

Until now there are no effective treatments available to attenuate inflammation and prevent kidney disease, hypertension, loss of vision, as well as other problems derived from inflammation induced by high circulating glucose values ​​in these patients.

For this reason, a research team from the University of Murcia and the Murcian Institute for Biosanitary Research (IMIB) is trying demonstrate the role of inflammasome activation in these diseases and to search for new drugs to inhibit the inflammasome and prevent the effects of chronic inflammation in diabetic patients.

The first step on this path is to know how the inflammasomes are activated. So your study, published in the magazine Science Advances, revealed that there are specific parts of these inflammasomes that are necessary to activate them. These results are very useful to control the activation of inflammasomes in different pathologies and diseases such as diabetes.

Until now, all the drugs that were being developed acted against a specific region, but the novelty of this study is based on the fact that a new region of that protein has been identified with an essential role in the activation of these inflammations. For this reason, the research opens the door to develop new drugs that act on that region.

Pablo Pelegrín Vivancos, Distinguished Researcher “Beatriz Galindo” in the Department of Biochemistry and Molecular Biology B and Immunology, University of Murcia; Diego Angosto Bazarra, Postdoctoral researcher, University of Murcia and Santiago Cuevas Gonzalez placeholder image, Principal Investigator, Cardiovascular and Renal Physiology, Molecular Inflammation Group, Murcian Institute for Biomedical Research (IMIB-Arrixaca), University of Murcia

This article was originally published on The Conversation. read the original.

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