Abstract
The neuropeptide oxytocin (OXT) and its receptor (OXTR) have recently been described in pancreatic islets. However, little is known about the function of pancreatic OXT or how it is regulated. In the present study, in vitro experiments using pancreatic rat islets and rodent beta-cell lines were conducted to expand current understanding of OXT signaling in the pancreas, particularly in the context of the stress response. OXT strongly potentiated insulin secretion in response to glucose in both rat islets and beta-cell lines, but only in the absence of norepinephrine (NE). Treatment with norepinephrine significantly downregulated OXTR mRNA expression in rat islets and beta-cell lines, and OXT mRNA expression in a mouse beta-cell line. OXT had no effect on oxidative or apoptotic processes in beta-cell lines exposed to metabolic stressors (e.g. hyperglycemia). An overarching model of OXT as a promoter of energy balance in the face of significant homeostatic challenges is proposed.