Researchers look at protein that may contribute to development of type 1 diabetes

Low levels of the protein interleukin-1 receptor antagonist (IL-1ra) may predict an increased risk of developing type 1 diabetes in children, according to a study currently being conducted by researchers at Georgia Health Sciences University.

The scientists believe that identifying young people whose genes put them at risk for type 1 diabetes at an early stage, before the disease has set in, may allow doctors to take preventative measures to keep those individuals from developing the metabolic condition.

IL-1ra has previously been shown to reduce inflammation. The researchers believed that failing levels of the protein may indicate that inflammation is increasing in the body and that the immune system may be about to attack the insulin-producing cells of the pancreas.

The investigators are currently following a group of children whose genes indicate that they may be at risk of developing type 1 diabetes, measuring the participants' blood levels IL-1ra and watching for signs of the metabolic disease. The team is also analyzing mice that were genetically programmed to lack the IL-1ra protein to see what effect this change has on insulin production.

In healthy individuals, the anti-inflammatory IL-1ra exists in balance with its counterpart, interleukin-1 beta (IL-1beta), which causes inflammation. However, the researchers believe that when IL-1ra levels drop, it allows IL-1beta levels to increase, leading to unchecked inflammation and damage to tissue in the pancreas.

"It's a balance; it's a competition," said Sharad Purohit, who is leading the research. "There is always a balance between beta cell production and destruction, and any process that can change the balance can push you to disease or help you recover from it."

The team believes that IL-1 inhibitors, which are already widely used to treat arthritis, may reduce the likelihood that a person with genetic susceptibility to type 1 diabetes will eventually develop the condition.