| First Author | Wee J | Year | 2021 |
| Journal | Cell Rep | Volume | 37 |
| Issue | 9 | Pages | 110067 |
| PubMed ID | 34852221 | Mgi Jnum | J:321562 |
| Mgi Id | MGI:6881789 | Doi | 10.1016/j.celrep.2021.110067 |
| Citation | Wee J, et al. (2021) Tentonin 3/TMEM150C regulates glucose-stimulated insulin secretion in pancreatic beta-cells. Cell Rep 37(9):110067 |
| abstractText | Glucose homeostasis is initially regulated by the pancreatic hormone insulin. Glucose-stimulated insulin secretion in beta-cells is composed of two cellular mechanisms: a high glucose concentration not only depolarizes the membrane potential of the beta-cells by ATP-sensitive K(+) channels but also induces cell inflation, which is sufficient to release insulin granules. However, the molecular identity of the stretch-activated cation channel responsible for the latter pathway remains unknown. Here, we demonstrate that Tentonin 3/TMEM150C (TTN3), a mechanosensitive channel, contributes to glucose-stimulated insulin secretion by mediating cation influx. TTN3 is expressed specifically in beta-cells and mediates cation currents to glucose and hypotonic stimulations. The glucose-induced depolarization, firing activity, and Ca(2+) influx of beta-cells were significantly lower in Ttn3(-/-) mice. More importantly, Ttn3(-/-) mice show impaired glucose tolerance with decreased insulin secretion in vivo. We propose that TTN3, as a stretch-activated cation channel, contributes to glucose-stimulated insulin secretion. |
