Type 2 diabetes is characterized by a deficit in-cell mass, impaired insulin secretion in re-sponse to various stimuli (1–3), as well as a variable extent of insulin resistance (4). More specifically, regarding-cell function, a significant reduction of the incretin effect, ie, the postprandial augmentation of insulin secretion by gut hormones, has been described in patients with type 2 diabetes (5). Thus, while the two incretin hormones gastric inhibitory polypeptide (glucose-dependent insulinotopic polypeptide [GIP]) and glucagon-like peptide 1 (GLP-1) are held responsible for 50–70% of the postprandial insulin responses in healthy individuals (6), their contribution to the overall insulin responses after oral glucose ingestion may amount to 20% in patients with type 2 diabetes (5, 7). The reasons underlying the loss of incretin activity in type 2 diabetes are still incompletely understood. The present article reviews the available evidence regarding disturbances in the enteroinsular axis in patients with type 2 diabetes and provides possible explanations for their etiologies, focusing on the personal experience of the authors.