The OADs are able, for a time, to reduce A1C but do not correct all the metabolic and glucoregulatory dysfunctions involved in type 2 diabetes pathophysiology. As a result, HbA1C goals become more difficult to maintain and a significant glycemic burden accumulates, increasing the risk of CV diseases. The treatment of co morbid conditions, particularly hypertension, may also impede achieving and maintaining glycemic goals. Difficulties in maintaining long-term glycemic control with currently available antidiabetic therapies have led to the need for additional treatments that can be used as monotherapy or combined safely with existing agents and that may target more of the underlying pathologies of type 2 diabetes.