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A possible treatment for one of the most common diseases in the world may have been discovered in a B.C. research lab.

In a study released Monday, researchers at the University of British Columbia (UBC) and Sweden’s Karolinska Institute found reducing or eliminating a specific protein in the fat cells of mice not only prevents the onset of Type 2 diabetes, but also appears to reverse the disease as well.

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That protein, dubbed CD248, was found to be higher in the fat cells of people with diabetes regardless of their shape and size, but would decrease to normal levels when people with obesity-associated diabetes reversed the disease through weight loss.

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Senior co-author Dr. Edward Conway, a professor in the faculty of medicine at UBC and a director of the Centre for Blood Research, is now hopeful the research could lead to a safe and effective new treatment.

“It’s early days but modifying the amount or function of CD248 in fat cells seems to be a promising new treatment strategy, an approach that may be eventually used by itself or with other drugs,” Conway said in a statement.

“The number of people with Type 2 diabetes is staggering, and as the incidence of obesity increases, more effective treatments for Type 2 diabetes are urgently needed.”

Type 2 diabetes impacts the way a person’s body metabolizes sugar, where the body is unable to properly use the insulin it produces or can’t produce enough.

Complications that can arise from Type 2 include heart and blood vessel diseases, stroke, kidney damage, poor skin wound healing, increased risk of infections and a higher incidence of some types of cancer.

Diabetes Canada says roughly 90 per cent of people living with diabetes has Type 2.

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The organization estimates 11 million Canadians are living with all forms of the disease, while Conway said more than 60 million adults are diagnosed across North America and Europe.

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A diabetes research group at Karolinska Institute used human genetic approaches to study the fat biopsies of patients who were thin, obese, diabetic and not diabetic.

While diabetes has typically been measured by how sensitive a person is to insulin, the researchers found studying the levels of the CD248 protein could be a more effective way to both predict who are at risk and the effectiveness of treatments.

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“This, together with experiments in which we reduced the CD248 gene in human fat cells, suggested that this approach improved fat tissue function, which could be relevant in future treatments of Type 2 diabetes,” said Dr. Mikael Rydén, who led the team at Karolinska Institute.

Back in Vancouver, Conway and his team obtained genetically-modified mice that lack CD248 only in the fat cells, and found it protected them from developing Type 2 diabetes.

Eliminating the protein altogether didn’t appear to result in any negative health outcomes, suggesting therapies to reduce the protein would be safe.

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“A most interesting finding was that the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese,” Conway said.

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The researchers added a new treatment based on their findings could still be a long way off.

“Our immediate goals are to understand how CD248 works so that safe and effective drugs that reduce the protein’s levels or that interfere with its function can be designed,” Conway said.