Obesity has been historically known as a risk factor for type 2 diabetes, and now a key mechanism has been found in the immune system that plays a part in the development of obesity-linked type 2 diabetes.
The outcome was found in a study led by researchers from King’s College London, UK and was published in the journal Cell Metabolism.
The findings are a stepping stone for new treatment methods and prevention of this health issue that has become extremely prevalent worldwide.
Internationally, approximately 371 million people are living with diabetes – 90% of these cases are type 2 diabetes. By the year 2030, there will be an estimated 550 million people with diabetes if this progression continues.
Since 1980, cases of diabetes have increased twofold – with 70 percent of the change happening because of aging populations around the world – while the other 30 percent are due to the rising incidence of risk factors, including obesity.
Previous research has shown the link between obesity and diabetes, but the molecules that cause this link have been a mystery.
The investigators studied mice that were genetically engineered to not have T-bet, a protein that controls the differentiation and function of immune cells. Researchers found that the mice had heightened insulin sensitivity, even though they were obese.
Dr. Howard explained:
“When T-bet was absent this altered the relationship between fat and insulin resistance: the mice had more intra-abdominal fat but were actually more sensitive to the glucose lowering effects of insulin. As fat accumulation in the abdomen is typically associated with worsening insulin resistance and other features of the metabolic syndrome, the findings seen were both unusual and unexpected.”
The researchers found that the intra-abdominal fat of these mice had fewer immune cells and was less swollen than that of regular mice. They further discovered that by moving immune cells that had no T-bet to younger, skinnier mice, the insulin sensitivity improved.
Professor Graham Lord added, “It appears that T-bet expression in the adaptive immune system is able to influence metabolic physiology.”
Generally, obesity is linked to insulin resistance and diabetes, however, this is not always the case. Many of the most common medications used to treat type 2 diabetes function by improving insulin sensitivity. More trials are needed to pinpoint other molecules in the pathway of action of T-bet, which could start the process for future drug options for the treatment of type 2 diabetes.
Giving specific immune cells as immunotherapy to better insulin resistance could also be a possibility for therapy in the future.
Dr. Howard concluded:
“This is just the start – the idea that the immune system can impact on metabolism is very exciting, but more research needs to be done before we can bring this work from the bench to the bedside for the benefit of patients.”
In January of this year, a study published in Nature suggested that a new new gene has been found that plays a role in insulin resistance and obesity – conditions that increase the risk of type 2 diabetes and heart disease.
Written by Kelly Fitzgerald