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Biomedical subjects

A Ohneda

Publications and source records attributed to A Ohneda.

At least 37 records · Page 2Linked to original sources
PubMed1989

Effect of porcine pancreastatin on endocrine function of canine pancreas.

Controversial results concerning the modulation of insulin release with pancreastatin prompted us to investigate the effect of this peptide upon the endocrine function of the pancreas using an in situ perfusion method in dogs. Administration of porcine pancreastatin into the pancreaticoduodenal artery in a dosage of 0.34 micrograms/kg of body weight during arginine infusion increased slightly plasma insulin and lowered minimally plasma glucagon in the pancreaticoduodenal vein. Pancreastatin infusion in a dosage of 500 ng/min did not modify glucose-induced insulin release and glucagon suppression by glucose. Theophylline infusion induced a slight increase in plasma insulin and glucagon in the pancreaticoduodenal vein. Pancreastatin infusion accelerated slightly these changes in plasma insulin and glucagon following theophylline infusion. From the present experiment it is concluded that porcine pancreastatin did not inhibit glucose-induced insulin release from the canine pancreas, inconsistent with the first report on insulin release from the rat pancreas. Alternatively, porcine pancreastatin rather stimulated insulin release during arginine infusion or following theophylline administration.

Animals↗
PubMed1988

Effect of intraluminal administration of amino acids upon plasma glicentin.

To see what effect intraluminal amino acids would have on glicentin secretion, we put a mixture of 10 amino acids (1 g/kg) into the duodenum of five normal, conscious piglets. Their plasma nitrogen rose, as did insulin and glucagon measured with C-terminal-specific antiserum. Plasma total immunoreactive glucagon, determined with non-specific antiserum, rose from 2753 +/- 460 pg/ml to a peak of 4434 +/- 1352 pg/ml at 30 min. Plasma glicentin, determined with R 64 antiserum, rose from a fasting level of 297 +/- 70 pmol/l to a peak of 702 +/- 167 pmol/l at 45 min. We also gave oral arginine to 6 pancreatectomized dogs to investigate why the plasma glicentin rises after amino acid ingestion. Arginine raised the plasma total immunoreactive glucagon from 1120 +/- 214 pg/ml to a peak of 2266 +/- 512 pg/ml at 45 min. We conclude that intraluminally administered amino acids enhance glicentin secretion from the gut.

Amino Acids↗
PubMed1988

Adrenergic modulation of pancreatic glucagon and insulin secretion in sheep.

The effect of intravenous infusion of epinephrine, either alone or together with various doses of phentolamine or propranolol, on the secretion of both glucagon and insulin was determined in six sheep. Intravenous infusion of epinephrine alone caused increases in plasma glucagon and glucose concentrations and produced a slight but significant decrease in plasma insulin concentration. The concomitant infusion of propranolol and epinephrine augmented glucagon release and inhibited insulin secretion. Combined propranolol plus epinephrine infusion also caused a marked hyperglycemia. The concomitant infusion of phentolamine and epinephrine produced slight inhibition of glucagon secretion and markedly promoted insulin secretion. Epinephrine-induced hyperglycemia was eliminated by phentolamine infusion. The effects of isoproterenol infusion on plasma glucagon, insulin, and glucose concentrations were similar to that caused by the concomitant infusion of phentolamine and epinephrine. The effects of isoproterenol were abolished by the infusion of propranolol. It is concluded that an alpha-receptor mechanism is the most important component of adrenergic modulation of pancreatic glucagon secretion, whereas beta-receptor activation stimulates and alpha-receptor activation inhibits insulin secretion in sheep.

Adrenergic alpha-Antagonists↗
PubMed1988

Effect of glicentin-related peptides upon the secretion of insulin and glucagon in the canine pancreas.

In order to clarify responses of the endocrine pancreas to glicentin, four glicentin-related peptides were investigated in a local circulation preparation of the canine pancreas. These peptides were administered in a dosage of 200 pmole for 10 min into the pancreaticoduodenal artery under the continuous infusion of 0.5% arginine solution. In a group of six dogs, the administration of glicentin-related pancreatic peptide (GRPP) and glicentin 1-16 resulted in an increase in plasma insulin (IRI) and a decrease in plasma glucagon (IRG). In the other group of six dogs, the administration of glicentin 62-69 induced an increase in plasma IRI and a decrease in plasma IRG. Following the successive infusion of oxyntomodulin, both plasma IRI and IRG increased slightly. Porcine glucagon administered at the end of each experiment exerted a rise in blood glucose and plasma IRI in addition to an increase in plasma IRG. In comparison of the maximal responses of plasma IRI and IRG to these glicentin-related peptides, the administration of glicentin 1-16, 62-69 or GRPP elicited an increase in plasma IRI and a decrease in plasma IRG. In contrast, oxyntomodulin and glucagon increased both plasma IRI and IRG. The present study indicates that glicentin-related peptides, both the N- and C-terminal portions, affect the endocrine function of the pancreas and suggests that glicentin released by nutrient ingestion plays an important role in the enteroinsular axis.

Animals↗
PubMed1987

The role of humoral factors and the ileocecal valve in pathological changes occurring after distal small bowel resection.

Experimental studies using dogs were performed to elucidate the participation of gastrointestinal hormones as well as the ileocecal valve in postoperative sequelae following massive small bowel resection. Although in both the ileal resection and the ileocecal resection groups the absorption of fat was reduced postoperatively, body weight tended to increase in the former, while it decreased gradually in the latter. In addition, watery diarrhea persisted after ileocecal resection. Plasma total bile acid concentrations in each group were lower than those before surgery, as were plasma levels of both total glucagon and neurotensin. Although differences were not significant, plasma neurotensin levels tended to be higher after ileocecal resection, but plasma total glucagon levels tended to be lower. Plasma gastric inhibitory polypeptide (GIP) response to butter ingestion was also lower after both ileal and ileocecal resection; especially in the latter case the decrease was significant. These results indicate that the diminished plasma levels of neurotensin, enteroglucagon and GIP may be related to the impairment of adaptive changes in the remaining small intestine.

Animals↗
PubMed1987

Effect of ileo-jejunal transposition on intestinal adaptation after total colectomy in dogs.

The effect of ileo-jejunal transposition (IJT) on the intestinal adaptation after total colectomy was investigated in 4 mongrel dogs. Hyperenteroglucagonemia was observed in the IJT with colectomy group, especially in postprandial state. Obvious hyperplastic changes were observed in all part of the small intestinal mucosa in the colectomy with IJT group. However, there were no significant differences in body weight changes between the colectomy with IJT group and the colectomy group. Postprandial plasma gastrin levels were lower in the colectomy with IJT group compared to the control. These results suggest that IJT causes hyperenteroglucagonemia and intestinal mucosal hypertrophy in colectomized dogs. Enteroglucagon may have an inhibitory effect on postprandial gastrin release.

Adaptation, Physiological↗
PubMed1987

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

In order to clarify the role of gastric inhibitory polypeptide (GIP) in an enteroinsular axis, 19 healthy mongrel dogs were divided into following groups: 5 normal dogs (N), 4 dogs with gastrojejunostomy (GJ), 5 dogs with duodenal fistula (D) and 5 vagotomized dogs (V). Four weeks after the operation glucose was administered orally or intraduodenally in a conscious state. In group D, glucose administration was repeated under atropine injection (A). Glucose-induced response of plasma GIP was exaggerated in all the groups compared with group N. The regression equation reported by Lauritsen and Moody was obtained in each dog from the ratio of plasma insulin to blood glucose and from plasma GIP. The slope of the regression line was elevated in group GJ and reduced in group V. However, groups D and A did not reveal any difference in the slope of the regression line compared with group N. From the present study, it might be concluded that the B-values in Lauritsen and Moody's equation indicates the sensitivity of the B cell in the pancreatic islet and that GIP secretion plays an important role in the glucose-induced insulin response even in the conditions with various surgical modifications.

Animals↗
PubMed1986

Effect of glicentin-related peptides on glucagon secretion in anaesthetized dogs.

Recent studies have demonstrated that glicentin is released during nutrient ingestion. However, the biological function of glicentin remains unclear. In order to clarify the role of glicentin in the enteroinsular axis, the effect of glicentin-related peptides was investigated using in vivo local circulation of canine pancreas. Peaks I and II of gut glucagon-like immunoreactivity, partially purified from porcine intestinal extract by affinity chromatography and gel filtration, synthesized hexadecapeptide of N-terminal glicentin (1-16) and synthesized octapeptide of C-terminal glicentin (62-69) were administered for 10 min into the pancreaticoduodenal artery of canine pancreas. Blood samples were then drawn from the pancreaticoduodenal vein. The administration of peak I of glucagon-like immunoreactivity during arginine infusion in a dosage of 20 ng reduced the glucagon secretion by 42 pmol/l (p less than 0.05), whereas peak II of glucagon-like immunoreactivity (20 ng) slightly increased the plasma level of insulin, although not significantly. The administration of glicentin (1-16) in a dosage of 400 ng during saline infusion did not alter the plasma insulin level, but reduced the plasma glucagon level in the pancreaticoduodenal vein by 29 pmol/l (p less than 0.05). In addition, glicentin [62-69] in a dosage of 400 ng exerted a decrease in both the plasma insulin (40 mU/l, p less than 0.05) and glucagon level (27 pmol/l, p less than 0.05). The present study demonstrates the suppression of pancreatic glucagon release during the infusion of peak I glucagon-like immunoreactivity and N- or C-terminal glicentin-related peptide. Therefore, it is suggested that glicentin released during nutrient intake might inhibit the secretion of glucagon.

Animals↗
PubMed1986

Adrenergic modulation of pancreatic glucagon and insulin secretion in goats.

Five goats were used to investigate adrenergic influences on the secretion of both glucagon and insulin. The secretion of glucagon was augmented via alpha-adrenergic stimulation. The secretion of insulin was enhanced by stimulation of beta-adrenergic receptors and inhibited by alpha-adrenergic stimulation.

Animals↗
PubMed1986

Gastric acid secretion and gut hormone release in patients undergoing pancreaticoduodenectomy.

The changes in gastric acid secretion and gut hormone release were investigated in 11 patients who underwent pancreaticoduodenectomy. The amount of acid output showed normoacidity before surgery and hypoacidity after surgery. No peptic ulcers were detectable after surgery. Plasma gastrin levels were markedly reduced after surgery both in the fasting state and after a test meal loading. Although fasting plasma levels of both gastric inhibitory polypeptide (GIP) and insulin after surgery were close to those before surgery, the response of these hormones to the meal was significantly reduced after surgery. On the other hand, blood glucose concentrations increased gradually after feeding, and the elevation was greatly prolonged after surgery compared with preoperative levels. From these results, it is concluded that peptic ulcer will not occur if subtotal gastrectomy is performed during Whipple's procedure. It is presumed that the diminished release of gut hormones such as gastrin, GIP, and insulin was due to the massive resection of the distal stomach, the upper small intestine, and the head of the pancreas and to the diversion of the stream of food from the duodenum to the jejunum. It is also assumed that the glucose-dependent insulinotropic action of GIP would be impaired by the procedure.

Adult↗
PubMed1985

Response of extrapancreatic glucagon to gastrointestinal hormones in pancreatectomized dogs.

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 micrograms/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 (0.5 microgram/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.

Animals↗
PubMed1985

Secretion of glucagon in liver cell carcinoma.

In order to elucidate the response of plasma glucagon in liver cell carcinoma, a clinical study was performed in 12 patients with liver cell carcinoma in addition to 8 patients with liver cirrhosis and 8 normal subjects. Arginine infusion elicited increases in plasma insulin and glucagon in 6 patients with liver cell carcinoma as well as 8 patients with liver cirrhosis compared with the controls. However, the responses of plasma insulin and glucagon in liver cell carcinoma did not exceed those in liver cirrhosis. No glucagon secreting cell was proved in the hepatic cancer tissues from two other patients. Furthermore, no measurable glucagon was demonstrated in the tumor tissues extracted from four other patients with liver cell carcinoma. The extract of the tumors, infused into the pancreatic artery of anesthetized dogs, did not elicit any discernible changes in glucagon and insulin in the pancreatic vein. The present study demonstrates an elevated response of plasma glucagon in liver cell carcinoma. Since the morphological and biochemical studies failed to demonstrate the glucagon secreting cell or glucagon-stimulating material in the tumor tissues, the elevated plasma glucagon response might be interpreted by the increased A-cell function of the pancreas and the decreased degradation of the hormones in the liver.

Aged↗
PubMed1985

Role of vagus nerve in secretion of gastric inhibitory polypeptide in dogs.

In order to clarify the role of the vagus nerve in the secretion of gastric inhibitory polypeptide (GIP), experiments were performed on dogs. Response of plasma GIP to intraduodenal instillation of glucose was slightly lower in a group which received atropine, than in a group of normal dogs. The response of plasma GIP to intraduodenal glucose load was not different between vagotomized dogs and normal dogs. Electric stimulation of the vagus nerve did not produce any significant changes in plasma GIP in anesthetized dogs. In conclusion, the present study indicates that the role of the vagus nerve on GIP secretion is tiny, if any, and that the nervous influence does not overcome the effect of intraluminal administration of glucose.

Animals↗
PubMed1985

Gastric acid secretion and gastrin and gastric inhibitory polypeptide release in cirrhotic patients.

Gastric acid secretion, incidence of gastric mucosal lesion, and gut hormone responses were studied in 24 patients with liver cirrhosis. Gastric acid output in these subjects showed normal acidity and was nearly similar to that in patients with gastric ulcer. The incidence of gastric mucosal lesion was high, especially in patients whose plasma disappearance rate of indocyanine green was low. Plasma levels of both gastrin and gastric inhibitory polypeptide were higher in cirrhotic patients than in control subjects both in the fasting state and after the ingestion of a test meal. Gel chromatography of the postprandial plasma of cirrhotics showed a higher immunoreactivity at the second peak than in controls. This is because cirrhotics have a higher percentage of authentic gastric inhibitory polypeptide, although the elution patterns were similar in both groups. It is suggested that impairment of extraction of some molecular components of both gastrin and gastric inhibitory polypeptide may occur in the cirrhotic liver.

Adult↗
PubMed1984

Insulin and glucagon in spontaneously diabetic non-obese mice.

To investigate the role of glucagon in the development of diabetes mellitus, spontaneously diabetic non-obese mice were studied before (group 1) and after the onset of diabetes mellitus (group 2). In group 1, fasting blood glucose and insulin in plasma and pancreas did not differ significantly, while plasma glucagon was elevated (48.9 +/- 10.4 versus control 18.6 +/- 6.0 pmol/l). In group 2, the insulin content of plasma and the pancreas were markedly reduced, whereas plasma glucagon was elevated (180.9 +/- 59.1 pmol/l). When diabetic mice were treated with insulin for 4 weeks (group 3), plasma glucagon was markedly reduced compared with that of group 2 (30.3 +/- 9.0 pmol/l). In group 1, glucagon and glucagon-like immunoreactivity of the intestine were reduced. The glucagon content of the intestine was elevated in group 2. Group 3 elicited increased contents of gastric glucagon as well as intestinal glucagon-like immunoreactivity. We conclude that, in addition to insulin deficiency, hypersecretion of glucagon might contribute to the development and clinical course of diabetes mellitus in the non-obese diabetic mouse.

Animals↗
PubMed1984

Response of gastric inhibitory polypeptide to fat ingestion in normal dogs.

Because of the differences in the data concerning the mechanism by which gastric inhibitory polypeptide (GIP) is secreted following fat ingestion, we were prompted to investigate the characteristics of the GIP response to the triacylglycerol components in normal dogs. Oral administration of glycerol (1 g/kg) slightly elevated the blood glucose levels but not the plasma GIP. Palmitate (1 g/kg) administration did not change the blood glucose whereas the plasma GIP was increased remarkably and remained elevated at 120 min. Oral administration of tricaprylin (2 g/kg) did not elicit any discernible changes in the blood glucose nor in the plasma GIP. Column chromatography of plasma obtained from a dog after palmitate ingestion revealed three GIP-immunoreactive peaks: one peak corresponding to the authentic GIP, one to the large molecular weight peak, and one to the small molecular weight peak. Similar results were obtained with the plasma collected after fat ingestion. From the present study, it would appear that hydrolysis of triacylglycerol plays an important role in GIP release from the intestine. Furthermore, it is concluded that the long chain fatty acids stimulate GIP release whereas the medium chain fatty acids do not.

Animals↗