Inflammation and Diabetes: A Surprising Connection?

Tissue inflammation and diabetes are both major issues affecting the American public, but chances are you probably don’t associate these two ailments with each other. The obvious reason for this is that, on the surface at least, diabetes and inflammation appear to be have little in common, afflicting different parts of the body and causing different symptoms. While the effects of these two conditions are vastly different, they may be much more closely related than you might think.

Contrasting Diabetes and Inflammation

Over the last several decades, diabetes has become a household word, with the number of people diagnosed with this condition soaring by 176% from 1980 to 2011. The vast majority of diabetics develop type 2 diabetes, which prevents the patient from properly managing their level of glucose (glucose is the term for the sugar in your bloodstream). Type 2 diabetes occurs when either one of two scenarios unfold:

• The body’s cells become immune to the effects of insulin, a condition referred to as insulin resistance. Insulin is a hormone that removes glucose from the bloodstream, allowing it to be stored for future use.
• The pancreas does not produce enough of insulin to clear excess glucose from the patient’s blood

Patients with type 2 diabetes are urged to closely monitor their diet, particularly with regard to carbohydrate consumption.

Though it is the often the source of much grief, inflammation is not inherently bad for your body. In fact, tissue inflammation is crucial weapon in the immune system’s arsenal. After sustaining a cut, sprain, burn or other types of physical injury, the body responds by swelling the afflicted tissues, thereby preventing harmful bacteria and other harmful substances from pouring into the wound.

 Unfortunately, unnecessary inflammation can also occur, oftentimes in patients with autoimmune disorders such as lupus and multiple sclerosis. In these situations, the body’s immune system mistakes normal cells as hostile invaders, and proceeds to attack them. As a result, certain tissues within the body can become inflamed, leading to other chronic health problems.

Researching the Issue – with Mice

In recent years, multiple studies have found a surprising link between these two seemingly unrelated issues. In 2007, a study issued by the University of California, San Diego (UCSD) School of Medicine noted the influence of a certain type of immune cell on insulin resistance. These cells are known as macrophages, and own the title of the biggest white blood cell in the body (although “big” in this case is a relative term – the average macrophage is only .00083 inches wide).  The UCSD team observed that macrophages secrete a certain type of protein, called cytokines, after entering various tissues. In turn, these cytokines interfere with the surrounding cells, rendering them impervious to the effects of insulin. This reaction occurred in muscle, fat and liver tissues.

To confirm their theory that macrophages are responsible for this chain reaction, the UCSD researchers set up an experiment using laboratory mice. During this procedure, the mice were subjected to an adoptive bone marrow transfer, which effectively crippled their ability to produce macrophages. The mice were then put on a diet consisting of high-fat foods. As was to be expected, these mice soon became obese, and also began to suffer from fatty liver disease. Despite their sizable weight gain, however, none of the test mice subsequently developed a resistance to insulin.

Roughly a year later, the UCSD School of Medicine produced another report covering much of the same territory. Released in October 2008, this study examined the effects of another type of inflammation-causing cell in obese mice. This time, the researchers focused on CD11c-positive cells, and sought to remove them from the bodies of their test subjects. To accomplish this goal, the UCSD team used a group of mice that had been genetically-altered to be sensitive to diphtheria toxins. In addition to causing diphtheria disease, these toxins also destroy CD11c-positive cells.

Like the mice in the 2007 study, the researchers fed their test mice a steady diet of fattening foods. After becoming obese and contracting type 2 diabetes, these mice were injected with the diphtheria toxin. Soon after the toxin was introduced into their bloodstream, the mice’s CD11c-positive cell count diminished rapidly, eventually killing off all of these cells inside the mice. The researchers found that the mice’s insulin resistance and diabetes symptoms disappeared with their CD11c-positive cells.

At the conclusion of both of the aforementioned studies, both researcher teams argued that neutralizing certain immune cells might prove to be an effective treatment method for diabetics. Of course, this theory needs to survive further testing in order to become an accepted medical fact. If the body’s inflammatory response can be firmly linked to type 2 diabetes, the treatment methods for diabetes might see some major changes in the future.