| First Author | Wang Y | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 779 |
| PubMed ID | 28396589 | Mgi Jnum | J:272327 |
| Mgi Id | MGI:6282518 | Doi | 10.1038/s41598-017-00900-7 |
| Citation | Wang Y, et al. (2017) Sphingosine kinase 1-interacting protein is a novel regulator of glucose-stimulated insulin secretion. Sci Rep 7(1):779 |
| abstractText | Glucose-stimulated insulin secretion (GSIS) is essential in keeping blood glucose levels within normal range. GSIS is impaired in type 2 diabetes, and its recovery is crucial in treatment of the disease. We find here that sphingosine kinase 1-interacting protein (SKIP, also called Sphkap) is highly expressed in pancreatic beta-cells but not in alpha-cells. Intraperitoneal glucose tolerance test showed that plasma glucose levels were decreased and insulin levels were increased in SKIP(-/-) mice compared to SKIP(+/+) mice, but exendin-4-enhanced insulin secretion was masked. GSIS was amplified more in SKIP(-/-) but exendin-4-enhanced insulin secretion was masked compared to that in SKIP(+/+) islets. The ATP and cAMP content were similarly increased in SKIP(+/+) and SKIP(-/-) islets; depolarization-evoked, PKA and cAMP-mediated insulin secretion were not affected. Inhibition of PDE activity equally augmented GSIS in SKIP(+/+) and SKIP(-/-) islets. These results indicate that SKIP modulates GSIS by a pathway distinct from that of cAMP-, PDE- and sphingosine kinase-dependent pathways. |
