| First Author | Fadzeyeva E | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 5 | Pages | 106748 |
| PubMed ID | 37216093 | Mgi Jnum | J:338920 |
| Mgi Id | MGI:7485366 | Doi | 10.1016/j.isci.2023.106748 |
| Citation | Fadzeyeva E, et al. (2023) Pancreas-derived DPP4 is not essential for glucose homeostasis under metabolic stress. iScience 26(5):106748 |
| abstractText | Mice systemically lacking dipeptidyl peptidase-4 (DPP4) have improved islet health, glucoregulation, and reduced obesity with high-fat diet (HFD) feeding compared to wild-type mice. Some, but not all, of this improvement can be linked to the loss of DPP4 in endothelial cells (ECs), pointing to the contribution of non-EC types. The importance of intra-islet signaling mediated by alpha to beta cell communication is becoming increasingly clear; thus, our objective was to determine if beta cell DPP4 regulates insulin secretion and glucose tolerance in HFD-fed mice by regulating the local concentrations of insulinotropic peptides. Using beta cell double incretin receptor knockout mice, beta cell- and pancreas-specific Dpp4(-/-) mice, we reveal that beta cell incretin receptors are necessary for DPP4 inhibitor effects. However, although beta cell DPP4 modestly contributes to high glucose (16.7 mM)-stimulated insulin secretion in isolated islets, it does not regulate whole-body glucose homeostasis. |
