| First Author | Honda A | Year | 2018 |
| Journal | Endocr J | Volume | 65 |
| Issue | 1 | Pages | 83-89 |
| PubMed ID | 28978813 | Mgi Jnum | J:275645 |
| Mgi Id | MGI:6313452 | Doi | 10.1507/endocrj.EJ17-0333 |
| Citation | Honda A, et al. (2018) Normal pancreatic beta-cell function in mice with RIP-Cre-mediated inactivation of p62/SQSTM1. Endocr J 65(1):83-89 |
| abstractText | Recent studies have suggested that decreased pancreatic beta-cell function and mass are common features of patients with type 2 diabetes mellitus. Pancreatic beta-cell homeostasis is regulated by various types of signaling molecules and stress responses. Sequestosome 1/p62 (SQSTM1, hereafter referred to as p62) is a ubiquitin-binding adaptor protein involved in cell signaling, oxidative stress, and autophagy. Because p62 appears to play an important role in maintaining mitochondrial quality control, it is possible that the loss of p62 in pancreatic beta cells contributes to mitochondrial dysfunction, and thus leading to impaired glucose tolerance. In this study we investigated the physiological roles of p62 by inactivating p62 in a beta-cell specific manner. We found that firstly, rat insulin-2 promoter-Cre (RIP-Cre)-mediated p62 inactivation did not cause body weight gain, although ubiquitous inactivation of p62 was previously shown to result in severe obesity. Secondly, we found no gross structural disorganization of the islets of p62-deficient mice. Consistent with normal islet morphology, no impairment in glucose tolerance was observed in mice with RIP-Cre-mediated p62 deletion. These results suggest that p62 is dispensable for normal islet organization and beta-cell function. |
