EFFECT OF OCTREOTIDE ON PANCREATIC ENDOCRINE FUNCTION IN PARTIAL PANCREATECTOMY

Octreotide acetate (Sandostatin), a long-acting somatostatin analogue, has been demonstrated to inhibit pancreatic exocrine secretion, The e ffect of octreotide acetate on pancreatic endocrine function in patien ts undergoing pancreas surgery or pancreas transplantation has not bee n as well described, nor have the clinical implications been studied a s systematically, This study was designed to investigate the effects o f octreotide acetate on glucose metabolism and endocrine function in a partial pancreatectomized canine model, simulating reduced islet cell reserve, Serum levels of glucose, insulin, and glucagon were determin ed at intervals over 2 hr following an intravenous glucose tolerance t est (0.5 g/kg intravenous bolus of 50% glucose) in: normal animals (Gr oup A, n = 5), normal animals pretreated with an intravenous bolus of 400 mu g of octreotide acetate (Group B, n = 5), partial pancreatectom ized animals (Group C, n = 5), and partial pancreatectomized animals p retreated with an intravenous bolus of 400 mu g of octreotide acetate (Group D, n = 5). Peak glucose concentration was significantly increas ed in Group D when compared to Group C (Group C = 304.2 +/- 13.5 mg/dl vs Group D = 353.2 +/- 12.9 mg/dl, P < 0.05), indicating an impairmen t of glucose metabolism by octreotide. In addition, octreotide signifi cantly decreased peak insulin release in the partial pancreatectomy gr oups (Group C = 129 +/- 12.9 mu U/ml vs Group D = 47.5 +/- 6.8 mu U/ml , P < 0.05), There were no significant differences in the rate of gluc ose utilization or glucagon concentrations among the groups. These res ults demonstrate that octreotide does result in insulin suppression, w ith a resultant increase in stimulated glucose concentrations, in a ca nine model of reduced islet cell mass, Further studies are required to determine the mechanism of action of octreotide on endocrine function in the setting of pancreas transplant. (C) 1996 Academic Press, Inc.