D. Rouiller

Gastric and Pancreatic Release of Somatostatin-like Immunoreactivity During the Gastric Phase of a Meal: Effects of Truncal Vagotomy and Atropine in the Anesthetized Dog

The postprandial release of gastric and pancreatic somatostatin-like immunoreactivity (SLI) was examined in anesthetized dogs during the gastric phase of a meal, and the role of vagal and atropine-sensitive mechanisms in the responses was assessed. The intragastric instillation of liver extract at pH 7 elicited a significant rise in antral vein SLI (∼300 pg/ml) and gastrin concentration. After truncal vagotomy, both baseline and postprandial antral vein SLI and gastrin concentration increased significantly compared with the control group. The infusion of atropine (100 μg/kg/h) abolished the postprandial rise in antral vein SLI but not in gastrin. The liver meal at pH 2 elicited a sustained sixfold greater rise of antral SLI (∼2000 pg/ml) than that at pH 7, while gastrin concentrations did not rise significantly. The latter antral SLI response was not influenced by truncal vagotomy, but atropine infusion reduced it by about 50%. In response to the meal at pH 7, fundic vein SLI concentrations rose by about 300 pg/ml. The rise was augmented slightly by truncal vagotomy but was abolished completely by atropine infusion. In response to the meal at pH 2, fundic SLI decreased sharply below baseline levels. The response was not altered significantly by vagotomy, but was reversed completely by atropine infusion, during which fundic vein SLI concentrations rose significantly. Pancreatic vein SLI concentrations rose by about 350 pg/ml in response to the gastric meal at pH 7. That rise was not altered significantly by vagotomy but was abolished by atropine infusion. In response to the meal at pH 2, pancreatic SLI concentrations rose by about 1000 pg/ml above baseline, significantly greater than the response to the meal at pH 7. The pancreatic vein SLI response to the meal at pH 2 was not altered by vagotomy. It was reduced considerably by atropine infusion. It is concluded that SLI is released from the antrum, fundus, and pancreas during the gastric phase of a meal and that these responses are modified by acidification of the intragastric contents and by truncal vagotomy and atropine infusion. The greatly augmented release of antral SLI in response to the acidified meal raises the possibility of a role for somatostatin in acid-induced suppression of gastrin release.

Effect of bombesin upon plasma somatostatin-like immunoreactivity, insulin and glucagon in normal and chemically sympathectomized dogs.

The present study was designed to determine the effects of intravenously infused bombesin (10 ng/kg/min) upon basal and postprandial plasma somatostatin-like immunoreactivity (SLI), glucagon, insulin and triglyceride levels in normal (n = 12) and chemically sympathectomized (n = 11) dogs. Basal plasma SLI, glucagon and insulin levels rose significantly during the infusion of bombesin in the normal dogs, and this was not altered by chemical sympathectomy. Bombesin infusion enhanced the postprandial SLI response, while attenuating the postprandial glucagon response by 50% and the insulin response in the early postprandial phase of the meal. Sympathectomy did not significantly alter the basal levels of these polypeptides, but augmented the postprandial plasma SLI response during the first 90 min, and reduced the postprandial glucagon response during the infusion of bombesin. The postprandial insulin response was not affected by sympathectomy. In both normal and chemically sympathectomized dogs the rise in postprandial triglyceride levels was attenuated by bombesin infusion.

Oral administration of somatostatin reduces postprandial plasma triglycerides, gastrin and gut glucagon-like immunoreactivity

Abstract The present study was designed to determine if orally administered somatostatin can reduce the postprandial rise in plasma triglycerides, gastrin, gut glucagon-like immunoreactivity (GLI) and the pancreatic hormones insulin and glucagon. Ten overnight fasted dogs were fed a fat-protein meal with or without 2 mg synthetic somatostatin, followed by another 2 mg somatostatin 90 min later. After the meal with somatostatin, postprandial plasma triglyceride levels were significantly lower for 5 hours, GLI levels for 3.5 hours and gastrin levels for 1 hour compared to the controls. Plasma insulin, glucagon and somatostatin-like immunoreactivity was not different from the control experiments. It is concluded that orally administered somatostatin lowers the postprandial levels of triglycerides, GLI and gastrin in dogs. This may have therapeutic implications for the management of gastrointestinal and metabolic disorders.

Role of histamine H2-receptors in gastric and pancreatic release of somatostatin-like immunoreactivity during the gastric phase of a meal

The present study was designed to determine the role of H2-receptors in the postprandial release of somatostatin-like immunoreactivity (SLI) from the gastric fundus and antrum and from the pancreas. In dogs subjected to laparotomy, the pylorus was bisected and a gastric fistula was created, following which 250 ml 20% liver extract (LE) at pH 7 or 2 were instilled intragastrically. In the fundic vein the incremental SLI rise in response to LE at pH 7 was 2423 plus or minus 540 pg/ml during a control infusion of saline and 4780 plus or minus 863 pg/ml during the infusion of cimetidine (1 mg/kg per h) (P less than 0.05). In the antral vein the incremental SLI in response to LE at pH 7 was 2182 plus or minus 530 pg/ml during the saline control but did not rise significantly during cimetidine infusion. In the pancreatic vein the incremental SLI level after LE at pH 7 was 1953 plus or minus 358 pg/ml in the control experiments and 4430 plus or minus 1024 pg/ml during cimetidine infusion (P less than 0.025). The incremental inferior vena cava SLI level was approximately 925 pg/ml in both groups (not significant). The instillation of LE at pH 2 during the saline control lowered fundic vein SLI by 500 pg/ml; this decline was abolished during cimetidine infusion. In the antral vein the incremental SLI level of 15 750 plus or minus 2514 pg/ml during saline was lowered to only 6728 plus or minus 2257 pg/ml during cimetidine (P less than 0.025). After LE at pH 2 the incremental pancreatic vein SLI level of 5641 plus or minus 1175 pg/ml during the control infusion was also significantly reduced to 2392 plus or minus 559 pg/ml by cimetidine (P less than 0.05). The incremental SLI in the inferior vena cava was reduced from 1270 plus or minus 280 pg/ml during saline to 680 plus or minus 190 pg/ml when cimetidine was infused (P less than 0.05). The present data suggest a histaminergic influence via stimulation of H2-receptors upon the regulation of gastric and pancreatic somatostatin release during the gastric phase of a meal.

Evidence for a regulatory role of the stomach in islet cell function

Abstract Recent studies have suggested that gastric factors other than gastrin may be released in response to gastric test meals and stimulate islet cell function. The present study was designed to examine this further. In anesthetised, laparotomized dogs with a bisected pylorus and a gastric fistula, a liver meal at pH 2 or pH 7 was instilled intragastrically. Although gastrin levels were lower with the acidified meal, inferior vena cava, insulin, glucagon and plasma glucose levels were significantly higher than after a meal at pH 7. These differences were not changed by truncal vagotomy. The differences in insulin or plasma glucose levels were not altered by infusion of atropine, although the difference in glucagon levels was reduced considerably. The present data suggest that factors other than gastrin and unrelated to the vagus or to atropine sensitive pathways are able to influence islet cell function and possibly glucose homeostasis.