Type 2 Diabetes

Type 2 diabetes is a rapidly growing disease burden among industrialized societies. New treatment options are needed to prevent progression of disease and loss of pancreatic function in type 2 diabetic patients. Systemic inflammation, with infiltration of white blood cells into adipose and pancreatic tissues, has emerged as a mechanism to help understand insulin resistance and loss of insulin production, respectively, in type 2 diabetics.

Type 2 diabetes is commonly associated with obesity. Obese adipose tissue is characterized by white blood cell infiltration. This chronic (sterile) inflammation of the adipose tissue is thought to reduce sensitivity to insulin, which is necessary to trigger adipose cells to take up sugar from the blood.

It is understood that the beta islet cells of the pancreas (ie. cells that produce insulin) are initially able to compensate for reduced insulin sensitivity in obese patients by increasing output of insulin. Eventually, however, pancreatic islet cells are no longer able to keep up with insulin demand. The increased load on the pancreas results in stress of the pancreas and an inflammatory process ensues in the pancreatic islet cells themselves. This inflammation contributes to loss of function in these cells and a collapse of insulin production, leading to insulin dependence.

Using our anti-IL-1α True Human™ antibody to block systemic inflammatory processes may provide a means to reduce white blood cell infiltration in adipose tissues. This could improve insulin sensitivity. Reducing white blood cell infiltration in the pancreas could also improve health and productivity of pancreatic beta cells.

The potential ability to treat the underlying mechanisms of insulin resistance and insulin output could make the anti-IL-1α monoclonal antibody a breakthrough in the treatment of Type 2 diabetes.