The global epidemic of type 2 diabetes is largely secondary to insulin resistance induced by obesity and sedentary lifestyles. Most insulin-resistant subjects are able to increase b-cell secretion to meet the increased insulin demand and do not develop diabetes. However, when b-cell compensation fails, type 2 diabetes develops (1,2). Understanding the mechanisms of this compensatory response is of fundamental importance to elucidate the pathophysiology of type 2 diabetes and has implications for the treatment of the disease.