Previous Exposure to Glucose Enhances Somatostatin Secretion from the Isolated Perfused Rat Pancreas

Previous exposure to glucose enhances insulin and depresses glucagon secretion by the pancreas. We have investigated whether secretion of somatostatin is also influenced by a glucose priming effect. In perfused rat pancreas from 36 h fasted rats a 5 min pulse of arginine (8 mmol/l) rapidly elicited a peak of somatostatin release. A similar somatostatin response was evoked by a second, identical, pulse of arginine after perfusion with “basal” glucose (3.9 mmol/l) for 45 min. On the other hand when 27.7 mmol/l D-glucose, was administered for 20 min between arginine pulses, there was significant stimulation of somatostatin secretion. When arginine was re-introduced 15 min after the cessation of the pulse of elevated glucose the magnitude of the arginine-induced peak (min 0–2 of stimulation) was increased from 16.2±4.1 to 33.1±4.7 pg/2 min, p<0.01, relative to the first stimulation with arginine. None of these effects of glucose could be reproduced by Dgalactose. The somatostatin response to arginine was higher in pancreata from fed than from 36 h fasted animals as was also basal release (22.8±5.0 vs 9.0±2.0 pg/min). In the fed state the response to the second pulse of arginine was however reduced by 50% after perfusion with “basal” glucose. This decrease in responsiveness was counteracted by perfusion with 27.7 mmol/l glucose for 20 min between the arginine pulses. It is concluded that previous exposure to an elevated concentration of glucose enhances D-cell responsiveness to arginine in the fasted as well as the fed state.