| First Author | Ben-Zvi D | Year | 2015 |
| Journal | Proc Natl Acad Sci U S A | Volume | 112 |
| Issue | 50 | Pages | 15498-503 |
| PubMed ID | 26621734 | Mgi Jnum | J:228198 |
| Mgi Id | MGI:5705660 | Doi | 10.1073/pnas.1513872112 |
| Citation | Ben-Zvi D, et al. (2015) Angptl4 links alpha-cell proliferation following glucagon receptor inhibition with adipose tissue triglyceride metabolism. Proc Natl Acad Sci U S A 112(50):15498-503 |
| abstractText | Type 2 diabetes is characterized by a reduction in insulin function and an increase in glucagon activity that together result in hyperglycemia. Glucagon receptor antagonists have been developed as drugs for diabetes; however, they often increase glucagon plasma levels and induce the proliferation of glucagon-secreting alpha-cells. We find that the secreted protein Angiopoietin-like 4 (Angptl4) is up-regulated via Ppargamma activation in white adipose tissue and plasma following an acute treatment with a glucagon receptor antagonist. Induction of adipose angptl4 and Angptl4 supplementation promote alpha-cell proliferation specifically. Finally, glucagon receptor antagonist improves glycemia in diet-induced obese angptl4 knockout mice without increasing glucagon levels or alpha-cell proliferation, underscoring the importance of this protein. Overall, we demonstrate that triglyceride metabolism in adipose tissue regulates alpha-cells in the endocrine pancreas. |
