| First Author | Zhu L | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Pages | 14295 | PubMed ID | 28145434 |
| Mgi Jnum | J:244048 | Mgi Id | MGI:5912827 |
| Doi | 10.1038/ncomms14295 | Citation | Zhu L, et al. (2017) beta-arrestin-2 is an essential regulator of pancreatic beta-cell function under physiological and pathophysiological conditions. Nat Commun 8:14295 |
| abstractText | beta-arrestins are critical signalling molecules that regulate many fundamental physiological functions including the maintenance of euglycemia and peripheral insulin sensitivity. Here we show that inactivation of the beta-arrestin-2 gene, barr2, in beta-cells of adult mice greatly impairs insulin release and glucose tolerance in mice fed with a calorie-rich diet. Both glucose and KCl-induced insulin secretion and calcium responses were profoundly reduced in beta-arrestin-2 (barr2) deficient beta-cells. In human beta-cells, barr2 knockdown abolished glucose-induced insulin secretion. We also show that the presence of barr2 is essential for proper CAMKII function in beta-cells. Importantly, overexpression of barr2 in beta-cells greatly ameliorates the metabolic deficits displayed by mice consuming a high-fat diet. Thus, our data identify barr2 as an important regulator of beta-cell function, which may serve as a new target to improve beta-cell function. |
