| First Author | Wewer Albrechtsen NJ | Year | 2016 |
| Journal | Cell Rep | Volume | 17 |
| Issue | 11 | Pages | 2845-2856 |
| PubMed ID | 27974199 | Mgi Jnum | J:241712 |
| Mgi Id | MGI:5903539 | Doi | 10.1016/j.celrep.2016.11.051 |
| Citation | Wewer Albrechtsen NJ, et al. (2016) Glucagon-like Peptide 1 Receptor Signaling in Acinar Cells Causes Growth-Dependent Release of Pancreatic Enzymes. Cell Rep 17(11):2845-2856 |
| abstractText | Incretin-based therapies are widely used for type 2 diabetes and now also for obesity, but they are associated with elevated plasma levels of pancreatic enzymes and perhaps a modestly increased risk of acute pancreatitis. However, little is known about the effects of the incretin hormone glucagon-like peptide 1 (GLP-1) on the exocrine pancreas. Here, we identify GLP-1 receptors on pancreatic acini and analyze the impact of receptor activation in humans, rodents, isolated acini, and cell lines from the exocrine pancreas. GLP-1 did not directly stimulate amylase or lipase release. However, we saw that GLP-1 induces phosphorylation of the epidermal growth factor receptor and activation of Foxo1, resulting in cell growth with concomitant enzyme release. Our work uncovers GLP-1-induced signaling pathways in the exocrine pancreas and suggests that increases in amylase and lipase levels in subjects treated with GLP-1 receptor agonists reflect adaptive growth rather than early-stage pancreatitis. |
