Response of gastric inhibitory polypeptide (GIP) to oral administration of nutrients in normal and pancreatectomized dogs

Ohneda, Akira; Kobayashi, Takashi; Nihei, Jiro

doi:10.1016/0167-0115(83)90257-4

Cited by 8 publications

(8 citation statements)

References 27 publications

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“…The response of gastric glucagon to GIP in their experiment resembles that of pancreatic glucagon (Dupre et al 1973;Ravinovitch and Dupre 1974). The previous study from our laboratory demonstrated that plasma GIP increased following oral administration of glucose in pancreatectomized dogs (Ohneda et al 1983). In this experiment, however, plasma glucagon (mostly extrapancreatic glucagon) did not change in spite of the increase of plasma GIP.…”

Section: Discussionmentioning

confidence: 37%

“…This result does not support the stimulation of extrapancreatic glucagon by endogenous GIP, although a possibility that extrapancreatic glucagon may be suppressed by hyperglycemia (Ohneda et al 1984) cannot be ruled out. Furthermore, oral administration of butter in combination with pancreatic enzymes induced a significant rise of plasma GIP in pancreatectomized dogs (Ohneda et al 1983). In this situation the plasma level of glucagon (probable extrapancreatic glucagon) did not change.…”

Section: Discussionmentioning

confidence: 87%

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Response of extrapancreatic glucagon to gastrointestinal hormones in pancreatectomized dogs.

Ohneda

Kobayashi

Nihei

1985

Tohoku J. Exp. Med.

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In order to investigate the effect of gastrointestinal hormones upon the secretion of extrapancreatic glucagon, tetragastrin, secretin, caerulein and cholecytokinin-pancreozymin octapeptide (CCK-octa) were administered during saline or arginine infusion in pancreatectomized dogs. Intravenous administration of tetragastrin (7 p g/kg) did not elicit any changes in plasma glucagon during saline infusion, while the plasma glucagon increased significantly following tetragastrin infusion during arginine infusion. The administration of secretin (3 U/kg) did not affect the plasma level of glucagon during saline or arginine infusion at all. Plasma glucagon did not change after the administration of caerulein (0.5pg/kg) during saline infusion, whereas it increased significantly following caerulein administration during arginine infusion. Intravenous administration of CCK-octa in a dose of 20 U/kg did not affect the plasma level of glucagon during saline infusion but exerted a significant rise of extrapancreatic glucagon during arginine infusion. It is concluded from the present experiment that the administration of tetragastrin, caerulein or CCK-octa enhances the release of extrapancreatic glucagon stimulated by arginine infusion while secretin infusion does not affect the secretion of extrapancreatic glucagon.tetragastrin ; secretin ; caerulein ; CCK-octapeptide ; arginine Since the establishment of the presence of extrapancreatic glucagon (Matsuyama and Foa 1974;Vranic et al. 1974), the regulation of extrapancreatic glucagon has been reported by many authors (Lefebvre and Luyckx 1981;Ohneda 1981). Among various factors, gastrointestinal factors have been considered to play an important role in the secretion of extrapancreatic glucagon. In a previous study from our laboratory it was demonstrated that extrapancreatic glucagon responds to intraluminal administration of glucose and arginine (Ohneda et al. 1984). Therefore, a participation of gastrointestinal hormones can be presumed in the regulation of extrapancreatic glucagon during nutrient ingestion. In this study, the effect of gastrointestinal hormones upon the secretion of extrapancreatic glucagon was investigated using pancreatectomized dogs.

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Section: Discussionmentioning

confidence: 37%

Section: Discussionmentioning

confidence: 87%

Response of extrapancreatic glucagon to gastrointestinal hormones in pancreatectomized dogs.

Ohneda

Kobayashi

Nihei

1985

Tohoku J. Exp. Med.

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“…Plasma insulin (IRI) was determined by the immunoassay using two antibody system (Morgan and Lazarow 1963). Plasma GIP was determined as described previously (Ohneda et al 1983), using antiserum R64, which was donated by Dr. A.J. Moody (Novo Institute, Bagsvaerd, Denmark).…”

Section: Methodsmentioning

confidence: 99%

“…Gastric inhibitory polypeptide (GIP) is widely distributed in the gut from the duodenum to the ileum, and it has been known that GIP is secreted by the intraluminal administration of glucose or fat . Furthermore, the concentration of plasma GIP is higher than that of secretin or PZ and resembles that of GLI (Ohneda et al 1983). Therefore, it is presumed that GIP might play an imporReceived September 16, 1986; accepted for publication December 3, 1986.…”

mentioning

confidence: 99%

“…These facts might suggest that GIP is closely related to the enteroinsular axis. In contrast, endogenous GIP released by fat ingestion did not appear to fully activate the enteroinsular axis in man (Sarson and Bloom 1981) and in dogs (Ohneda et al 1983). Therefore, in order to clarify the role of GIP in the enteroinsular axis, the present study was carried out to see if the secretion of insulin is altered in the states with elevated GIP in various animal models.…”

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confidence: 99%

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Glucose-induced responses of insulin and gastric inhibitory polypeptide in various animal models.

Ohneda

Kobayashi

Nihei

1987

Tohoku J. Exp. Med.

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An experimental study on the gastric acid and gut hormone secretion after pylorus preserving duodenectomy in dogs

et al. 1992

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To clarify changes in gastric acid and gut hormone secretion after pylorus-preserving pancreaticoduodenectomy (PPPD), an experimental study was performed using a model of pylorus-preserving duodenectomy in dogs previously provided with Heidenhain pouch (HP). The duodenectomy involves resection of the duodenum and 10 cm of the proximal jejunum preserving 2 cm of juxtapyloric duodenum and round-shaped duodenal wall around pancreatic papilla. Reconstruction was done by anastomosing the rho-shaped jejunal loop to gallbladder, juxtapyloric duodenum and peripapillar round-shaped duodenal wall with ligation of the common bile duct. For these dogs, intravenous glucose tolerance test (IVGTT), oral glucose tolerance test (OGTT), meal ingestion test (TM) and histological studies of pancreatic specimen obtained at autopsy were performed investigating pancreatic, gastric acid and gut hormone secretion. Preservation of endocrine and exocrine pancreatic secretion after operation demonstrated our experimental model to be adequate for evaluation of the factor of duodenectomy in PPPD on gastric acid and gut hormone secretion avoiding the influences of changes in pancreatic secretion. Postprandial gastric acid secretion from HP did not change significantly after operation. Postprandial secretion of gastrin, glucagon, GIP and enteroglucagon did not alter significantly after operation. These results indicated that in the clinical PPPD procedure, preservation of more than 2 cm of duodenum from the pylorus produced neither postprandial gastric acid hypersecretion, which might be cause of postoperative stomal ulcer, nor any change of related gut hormone secretion.

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Response of gastric inhibitory polypeptide (GIP) to oral administration of nutrients in normal and pancreatectomized dogs

Cited by 8 publications

References 27 publications

Response of extrapancreatic glucagon to gastrointestinal hormones in pancreatectomized dogs.

Response of extrapancreatic glucagon to gastrointestinal hormones in pancreatectomized dogs.

Glucose-induced responses of insulin and gastric inhibitory polypeptide in various animal models.

An experimental study on the gastric acid and gut hormone secretion after pylorus preserving duodenectomy in dogs

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