The early studies by Nauck and Holst have shown that the actions of GLP-1 and GIP on insulin secretion are nearly equal and additive in healthy humans [20,21], which is not observed in the set of T2D where the endocrine pancreas ceases responsiveness to GIP but remains responsive to GLP-1, explaining the reduced/absent incretin effect of GIP in T2D [22,23]. Here, GIP is linked to type 2 diabetes mellitus.