The present invention discloses a method for therapeutically treating mammals, including but not limited to humans, to increase the relative insulin producing performance of endogenous pancreatic ²-cells and to cause differentiation of pancreatic epithelial cells into insulin producing ²-cells. Oral administration of a DP-IV inhibitor causes the active form of GLP-1 to be preserved longer under physiological conditions. The extended presence of GLP-1, in particular in the pancreatic tissue facilitates differentiation and regeneration of the ²-cells already present that arc in need of repair. These repaired insulin producing cells can contribute to the correction and maintenance of normal physiological glycemic levels.
