Researchers say they have discovered a molecular link between obesity and type 2 diabetes, and the link could be a potential target for new drugs to treat the disease.
The researchers found that a protein released by fat tissue in mice causes insulin resistance, a primary risk factor for diabetes, elevated levels of the protein had previously been detected in patients suffering from the disease.
According to Dr Barbara Kahn of Beth Israel Deaconess Medical Center in Boston, Massachusetts, and lead author of the study, being resistant to insulin is one of the major causes of diabetes, and a major risk factor for heart disease and early mortality.
The pancreas, produces insulin and regulates blood sugar levels, and in people with type 1 diabetes, which accounts for 10-25 percent of cases, it does not produce any insulin which helps glucose, or sugar, from food get into cells.
The most common form of the disease, type 2 diabetes is caused by an inability to make enough, or to properly use, insulin, and it is estimated that about 90 percent of diabetes sufferers have type 2, which is linked to being overweight or obese.
According to the World Health Organization, about 150 million people worldwide suffer from diabetes and the number is expected to double by 2025.
Dr Kahn's team found the protein, called retinol binding protein (RBP4), by studying mice which had been genetically engineered to over or under produce another protein linked to insulin resistance.
The team also discovered that increasing levels of RBP4 caused insulin resistance while decreasing levels relieved the condition.
In people who are obese, or suffer from type 2 diabetes, excess amounts of RBP4 are linked to the severity of insulin resistance.
Khan says there is a rapidly increasing epidemic of obesity and type 2 diabetes in the western world, and clearly more effective treatment strategies are needed to prevent and treat diabetes.
She says RBP4 could prove to be a novel target for developing anti-diabetic therapies.
The research is published in the science journal Nature.