By Eddie Fatakhov M.D.
A study released out of a British Columbia research lab in Canada provided a new possible treatment for one of the most rampant diseases in the world. The study found that manipulation of a specific protein within fat cells may not only prevent the development of, but also reverse type 2 diabetes.
Type 2 diabetes now affects over 30 million Americans, according to the Centers for Disease Control and Prevention (CDC). The CDC estimates 84 million Americans are prediabetic (majority of them being unaware). Long-term complications of unmanaged type 2 diabetes can lead to heart disease, uncontrolled blood pressure, and nerve damage leading to limb amputation, kidney disease and blindness. Obesity is a primary risk factor of type 2 diabetes. The steady incline of obesity rates is directly correlating with the number of people being diagnosed with type 2 diabetes.
Our bodies are designed to eat in order to produce the energy we need to survive. Glucose (or blood sugar) is the body’s main source of fuel. We produce insulin in response to sugar consumption. Insulin is essentially the key that opens the doors for glucose to enter our body’s cells and fuel our body. When we regularly consume more glucose than required for the energy we expend, our body cannot keep up with the insulin demand and we can become insulin resistant. This results in an inability to use glucose for fuel. In turn, the glucose remains in the bloodstream, resulting in high blood sugar levels over long periods of time, eventually turning into, you got it… type 2 diabetes.
Along with potential insulin resistance, eating more than our body needs results in the expansion of white adipose tissue, where excess energy is stored as fat. This study conducted by a group of researchers out of Canada and Sweden examined a specific protein and its role in fat cells. This protein is a glycoprotein known as CD248, a protein that has a known association with the growth of tumours and inflammation. CD248 had never been studied in direct relation with obesity or insulin resistance. Researchers found that CD248 was found in greater amounts within the white adipose tissue in people that were obese or insulin resistant.
In a laboratory setting, researchers then artificially reduced the activity of CD248 in the white adipose tissue cells. From experimentation with the activity of CD248 in the white adipose tissue, researchers were able to conclude that the protein plays a role in the process that leads to insulin resistance and a cellular hallmark of obesity and hypoxia. Researchers next moved from the artificial reduction of activity to looking at the gene that codes for CD248 in mice. They used genetically-altered mice that lacked the gene that codes CD248 in white adipose tissue. These mice were fed high-fat diets and became obese, but did not develop insulin resistance and type 2 diabetes.
Potentially the most beneficial find is that the mice that already had diabetes and had the CD248 levels within their fat reduced, showed improvement in their insulin sensitivity. This discovery suggests the possibility of a future target therapy for type 2 diabetes, especially considering the reduction of CD248 did not result in any adverse events. Researchers are careful to point out that this is a very early stage of discovery, but the results give them a new pathway to head down in the treatment and/or prevention of type 2 diabetes. The more the prevalence of type 2 diabetes increases, the more urgent new treatment options become.