| First Author | Ahn C | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 10 | Pages | e0164527 |
| PubMed ID | 27736926 | Mgi Jnum | J:251728 |
| Mgi Id | MGI:6099307 | Doi | 10.1371/journal.pone.0164527 |
| Citation | Ahn C, et al. (2016) Calbindin-D9k Ablation Disrupt Glucose/Pancreatic Insulin Homeostasis. PLoS One 11(10):e0164527 |
| abstractText | It has been proposed that cellular Ca2+ signals activate hormone secretion. In pancreatic beta cells, which produce insulin, Ca2+ signals have been known to contribute to insulin secretion. Prior to this study, we confirmed that insulin-secreting beta cells express CaBP-9k, and assumed that CaBP-9k play a role in beta cell insulin synthesis or secretion. Using CaBP-9k knock out (KO) mice, we demonstrated that ablation of CaBP-9k causes reducing insulin secretion and increasing serum glucose. To compare the role of CaBP-9k with pathophysiological conditions, we exposed wild-type and CaBP-9k KO mice to hypoxic conditions for 10 days. Hypoxia induced endoplasmic reticulum (ER) stress, increasing both insulin signaling and insulin resistance. By exposing hypoxia, CaBP-9k KO mice showed an increased level of ER stress marker protein relative to wild type mice. Without hypoxic conditions, CaBP-9K ablation regulates calcium channels and causes ER stress in a CaBP-9K specific manner. Ablation of CaBP-9k also showed decreased levels of sulfonylurea receptor1 (SUR1) and inward-rectifier potassium ion channel 6.2 (Kir6.2), which are insulin secretion marker genes. Overall, the results of the present study demonstrated that CaBP-9k regulates synthesis of insulin and is part of the insulin-secreting calcium signaling. |
