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Biomedical subjects

T Taminato

Publications and source records attributed to T Taminato.

At least 73 records · Page 4Linked to original sources
PubMed1981

Immunoreactive somatostatin in human pancreatic secretion.

Somatostatin in human pancreatic juice collected during endoscopic retrograde cholangiopancreatography following secretin injection was determined by RIA. The mean immunoreactive somatostatin (IRS) levels in the pancreatic juice of 13 non-diabetics was 78 +/- 11 (SE) pg/ml. The IRS levels in 4 non-insulin-dependent diabetics ranged from 843 to 2286 pg/ml with a mean of 1559 +/- 392 (SE) pg/ml. This was significantly greater than non-diabetic values. The IRS in the pancreatic juice was immunologically indistinguishable from somatostatin14 but consisted of 2 major components, one corresponding to somatostatin14 and the other being of a molecular size of approximately 3000 daltons.

Adult↗
PubMed1981

Concentration and secretion of gastric somatostatin in streptozotocin-diabetic rats.

Both the release and the content of gastric somatostatin were investigated in streptozotocin-diabetic rats. Fundic and antral somatostatin contents were both increased in streptozotocin-diabetic rats compared with control animals. Basal somatostatin levels in the perfusates of streptozotocin-treated animals were not significantly different from those of the control animals. However, the peak values of somatostatin release induced by 5 x 10(-9) M glucagon in the diabetic animals were significantly higher than those of the controls. These results lead us to conclude that a hyperfunctioning state of the gastric D-Cells exists in hypoinsulinemic diabetes.

Animals↗
PubMed1981

Reversal of increased gastric somatostatin in streptozotocin-diabetic rats by whole pancreas transplantation.

Changes in both the content and the release of gastric somatostatin after amelioration of streptozotocin (SZ)-induced diabetes by whole pancreas transplantation were investigated in the present study. Highly inbred male Lewis rats were divided into three groups: normal, control rats; SZ-induced diabetic rats; and SZ-diabetic rats after whole pancreas transplantation. Fundic as well as antral somatostatin content in the streptozotocin-diabetic rats was significantly increased compared with the controls. Whole pancreas transplantation in SZ-diabetic rats markedly lowered the increased somatostatin content both in the fundus and the antrum. On the other hand, the exaggerated somatostatin release induced by glucagon from the isolated, perfused stomach observed in the SZ-diabetic rats was reduced to the level of normal rats by whole pancreatic transplantation. From these results, it is concluded that the hyperfunction of gastric D-cells in the SZ-diabetic rats is reversed by transplantation of whole pancreas.

Animals↗
PubMed1981

Effect of antisomatostatin gamma-globulin on gastrin release in rats.

In order to determine the mechanism of endogenous gastric somatostatin in the regulation of gastrin release, antisomatostatin rabbit gamma-globulin was administered in vivo and in vitro in the rat. First, in rats anesthetized by chloral hydrate, intravenous injection of 1 ml antisomatostatin rabbit gamma-globulin had no significant effect on plasma gastrin levels. Second, basal gastrin release from the isolated perfused rat stomach was not affected by the administration of antisomatostatin rabbit gamma-globulin (1:99 and 1:1 dilutions). Third, the addition of antisomatostatin rabbit gamma-globulin (1:99) to incubated rat antral mucosa, however, significantly increased the basal gastrin release. From these results, it is concluded that antral somatostatin exerts its inhibitory effect on basal gastrin release mainly not through the circulation but via paracrine pathways.

Animals↗
PubMed1980

Effects of [Asu1,7]-eel calcitonin on gastric somatostatin and gastrin release.

Effects of [Asu1,7]-eel calcitonin on gastric somatostatin and gastrin secretion were studied by using the isolated perfused rat stomach. [Asu1,7]-eel calcitonin (10(-9)--10(-7)M) caused a simultaneous dose-dependent increase of gastric somatostatin release and decrease of gastrin secretion, with a significant correlation between these two. The demonstration of calcitonin stimulation of gastric somatostatin release raises the possibility of somatostatin-mediated suppression of gastrin secretion by calcitonin.

Animals↗
PubMed1980

Effects of various gastrointestinal peptides on gastric somatostatin release.

Effects of various gastrointestinal peptides on gastric somatostatin release from the isolated perfused rat stomach were studied. After isolation of the stomach in a fasted rat by the method of Lefébvre and preperfusion with 4.6% dextran-Krebs-Ringer bicarbonate buffer containing 5.5 mM glucose, each peptide was infused into the left gastric artery at a constant rate for 15 min. Secretin and bombesin caused a significant increase of gastric somatostatin release in a dose-related manner (10(-8)-10(-6) M). Gastric somatostatin release was also stimulated after the administration of pentagastrin (10(-8)-10(-6) M). In contrast, both methionine-enkephalin and substance P decreased gastric somatostatin release in a dose-related manner (10(-8)-10(-6) M), whereas neurotensin (10(-8)-10(-6) M) failed to change it significantly. The present results suggest that these various gastrointestinal peptides may regulate gastric somatostatin secretion.

Animals↗
PubMed1980

Somatostatin release from the isolated, perfused diabetic rat pancreas: inverse relationship between pancreatic somatostatin and insulin.

The changes in pancreatic somatostatin content and release were studied in streptozotocin (STZ)-diabetic rats. Male Wistar rats were treated with a graded dose of STZ (group I, 0; II, 25; III, 50; IV, 75 mg/kg), which produced various grades of diabetic rats four weeks later. The pancreatic somatostatin content increased in proportion to the dose of STZ (I, 189 +/- 31; II, 222 +/- 20, III, 343 +/- 4; IV, 515 +/- 36 ng/g wet wt), while graded reductions of insulin content were observed. Significant increases in glucagon content were found only in groups III and IV. Pancreatic somatostatin release increased during arginine infusion (19.2 mM) dose dependently, (I, 543 +/- 36; II, 946 +/- 64; III, 1229 +/- 55; IV, 2186 +/- 150 pg/15 min), and it correlated with the graded decreases of insulin release. The glucagon release induced by arginine, however, did not change significantly. These results indicate that pancreatic somatostatin content and release increased in STZ-diabetic rats in proportion to the degree of insulin deficiency.

Animals↗
PubMed1980

Effects of insulin and pancreatic polypeptide on gastric somatostatin release.

Effects of arginine and such pancreatic hormones as insulin and pancreatic polypeptide on gastric somatostatin release from the isolated perfused rat stomach were studied. The stomach was isolated from a fasted rat by a modification of the method of Lefébvre and was perfused with 4.6% dextran Krebs-Ringer biocarbonate buffer containing 5.5 mM glucose. Both insulin and pancreatic polypeptide (10(-10), 10(-9), and 10(-8) M) caused a significant decrease in gastric somatostatin secretion. Insulin (10(-10) M), furthermore, inhibited the glucagon (5 x 10(-8) M)-induced somatostatin response. Arginine (10 and 19 mM) failed to elicit any significant change of somatostatin release. These results suggest that gastric somatostatin release is affected by pancreatic hormones.

Animals↗
PubMed1980

Reversal of the enhanced somatostatin release from the isolated, perfused diabetic rat pancreas after the amelioration of diabetes by whole pancreas transplantation.

To investigate the pancreatic endocrine function in streptozotocin-diabetic rats before and after the whole pancreas was transplanted, pancreatic insulin, glucagon, and somatostatin content and release were measured. Highly inbred Lewis male rats were divided into the following three groups: normal control rats; streptozotocin-induced-diabetic rats; and streptozotocin-diabetic rats transplanted with whole pancreas. Studies in vivo revealed normalization of elevated blood glucose and marked improvement of the impaired arginine-induced plasma insulin release by the transplantation of a healthy pancreas into the diabetic rats. Neither basal nor arginine-induced plasma glucagon levels in the diabetic rats were significantly different from the normal group, but significantly higher plasma glucagon levels were found in the transplanted rats. Studies in vitro using the isolated perfused rat pancreas revealed a significant increase of somatostatin release from the diabetic pancreas, with a marked reduction of insulin release and almost normal glucagon release. In the transplanted rats, on the other hand, arginine-induced somatostatin release from the host pancreas was reduced to normal without a significant change in insulin or glucagon release. In addition, the endocrine function of the graft remained normal in the transplanted rats. Pancreatic somatostatin release, thus, appears to be effected by changes in circulating insulin, since pancreatic transplantation effectively corrects the circulating insulin level.

Animals↗
PubMed1980

Effects of glucagon, secretin, and vasoactive intestinal polypeptide on gastric somatostatin and gastrin release from isolated perfused rat stomach.

To investigate the role of gastric somatostatin on gastrin secretion, glucagon, secretin, and vasoactive intestinal polypeptide (VIP) were perfused in the isolated pancreas-spleen-duodenum deprived preparation of rat stomach. After a preperfusion with 4.6% dextran Krebs-Ringer bicarbonate buffer containing 5.5 mM glucose, glucagon, secretin, and VIP at the concentrations of 10(-8), 10(-7), and 10(-6) M were infused into the left gastric artery at a constant flow of 2 ml/min for 15 min. All glucagon, secretin, and VIP evoked dose-dependent increases of somatostatin secretion with a simultaneous dose-related decrease of gastrin release. Furthermore, a significant correlation was found between the increase of somatostatin release and the decrease of gastrin secretion induced by glucagon, secretin, and VIP. These results raise the possibility that the suppression of gastrin secretion induced by glucagon, secretin, and VIP may, at least in part, be mediated by local action of gastric somatostatin.

Animals↗
PubMed1980

Effect of adrenergic blocking agents on plasma gastrin and secretin levels in man.

The effect of adrenergic blocking agents on gastrin and secretin secretion before and after a bolus arginine injection (arginine pulse) was investigated in normal subjects. Repeated arginine pulses given at 30-minute intervals caused abrupt and almost identical rises of plasma gastrin with each pulse. On the other hand, plasma secretin levels were unchanged by repeated injections of arginine. The increase in plasma gastrin induced by arginine pulse was significantly suppressed by the infusion of beta-adrenergic blocking agent, propranolol, while the infusion of alpha-adrenergic blocking agent, phentolamine tended to enhance the arginine-induced gastrin secretion slightly but not significantly. Whereas, the infusion of neither phentolamine nor propranolol had significant influence on secretin secretion. These results suggest that alpha- and beta-adrenergic receptors play an important role in the regulation of arginine-induced gastrin secretion.

Adrenergic alpha-Antagonists↗
PubMed1979

Theophylline: potentiation of arginine-induced somatostatin release from the isolated rat pancreas.

Somatostatin's release from the isolated rat pancreas was studied using a perfusion technique. Arginine at a concentration of 19 mM produced a biphasic increase in somatostatin release from the perfused rat pancreas. Both first and second phases of somatostatin's increase are significantly higher in the presence of 1 mM theophylline than in the absence of the drug. These results indicate the possible inclusion of the adenylate cyclase--cyclic AMP system in the regulatory mechanism of rat pancreatic somatostatin secretion.

Animals↗
PubMed1979

Somatostatin release from isolated perfused rat pancreas. Possible role of endogenous somatostatin on insulin release.

In order to elucidate the role of endogenous somatostatin in the control of insulin and glucagon secretion, glucagon- or insulin-induced somatostatin release from the isolated perfused rat pancreas was studied. Immunoreactive somatostatin was persistently released for 60 min in response to perfusion by 5.5 mM glucose at concentrations ranging between 10 and 15 pg/ml. The addition of glucagon (10(-8), 10(-7), and 10(-6) M) caused a dose-related increase of somatostatin release. In contrast, insulin release, especially its first phase, was suppressed when concentrations of glucagon were increased. The addition of insulin (10(-7) M and 10(-6) M) had no significant effect on somatostatin and glucagon release. These results raise the possibility that endogenous somatostatin and glucagon together regulate insulin secretion, suggesting a close interrelationship between insulin, glucagon, and somatostatin secretion within the islet.

Animals↗