| First Author | Yang Y | Year | 2019 |
| Journal | J Physiol Sci | Volume | 69 |
| Issue | 5 | Pages | 733-739 |
| PubMed ID | 31228099 | Mgi Jnum | J:289280 |
| Mgi Id | MGI:6434942 | Doi | 10.1007/s12576-019-00689-2 |
| Citation | Yang Y, et al. (2019) Islet beta-cell-produced NUCB2/nesfatin-1 maintains insulin secretion and glycemia along with suppressing UCP-2 in beta-cells. J Physiol Sci 69(5):733-739 |
| abstractText | Nesfatin-1 is a hypothalamic anorexigenic peptide processed from nucleobindin 2 (NUCB2). Central and peripheral administration of NUCB2/nesfatin-1 enhances glucose metabolism and insulin release. NUCB2/nesfatin-1 is also localized in pancreatic islets, while its function remains unknown. To explore the role of pancreatic beta-cell-produced NUCB2/nesfatin-1, we developed pancreatic beta-cell-specific NUCB2 knockout (betaNUCB2 KO) mice and NUCB2 gene knockdown (shNUCB2) MIN6 beta-cell line. In betaNUCB2 KO mice, casual blood glucose was elevated from 12 weeks of age. In a glucose tolerance test at 12 weeks, insulin secretion at 15 min was reduced and blood glucose at 2 h increased in betaNUCB2 KO mice fasted 8 h. In islets isolated from betaNUCB2 KO mice, high glucose-stimulated insulin secretion (GSIS) was impaired. In shNUCB2 MIN6 cells, GSIS was reduced and UCP-2 mRNA expression was elevated. These results show impaired GSIS possibly associated with UCP-2 overexpression in NUCB2-silenced beta-cells, suggesting that beta-cell-produced NUCB2/nesfatin-1 maintains GSIS and thereby glycemia. |
