Beta-endorphin is present in the endocrine pancreas, suggesting that endorphins may have a role in islet-cell function. To evaluate this possibility, we infused synthetic human beta-endorphin intravenously in healthy volunteers and in insulin-dependent diabetic patients. In both groups, beta-endorphin increased plasma glucagon concentrations, and this rise was accompanied by a significant increase in plasma glucose concentrations. In nondiabetic subjects, beta-endorphin also increased plasma insulin concentrations. The threshold dose of beta-endorphin for producing increased plasma concentrations of glucose and glucagon was 0.005 mg — a dose that acutely increased plasma concentrations of beta-endorphin by approximately 40-fold. Glucose, glucagon, and insulin responses to beta-endorphin could not be blocked by intravenous naloxone. These studies suggest that endorphins may be involved in glucoregulation, that their hyperglycemic action is mediated at least in part by glucagon, and that the effect of beta-endorphin on islet-cell function is relatively resistant to naloxone. (N Engl J Med. 1983; 308:349–53.) ENDORPHINS are endogenous opiate-like peptides that are released in conjunction with ACTH from the pituitary gland into the systemic circulation under certain conditions, such as those accompanying stress.1 The peripheral targets of endorphins that are released from the pituitary are uncertain. However, recent studies in the isolated perfused dog pancreas2 and in human beings3 suggest that endogenous opiates may play a part in islet-cell function. Moreover, there is recent evidence to suggest that beta-endorphin is produced in the pancreatic islets,4 so that endorphin may affect the endocrine pancreas by local as well as by humoral pathways. We have found that.
ASJC Scopus subject areas