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Biomedical subjects

A Goto

Publications and source records attributed to A Goto.

At least 325 records · Page 18Linked to original sources
PubMed1978

The effects of xenopsin of endocrine pancreas and gastric antrum in dogs.

Effects of synthetic xenopsin on endocrine pancreas and gastric antrum in anesthetized dogs were studied. Synthetic xenopsin was administered into the superior pancreaticoduodenal artery and plasma insulin, glucagon and gastrin in the superior pancreaticoduodenal vein and gastrin in the right gastroepiploic vein were measured radioimmunologically. Administration of 10 microgram of xenopsin per kg of body weight brought about a hyperglycemic response and rapid and sharp elevations of the hormones in the pancreatic vein. Plasma gastrin level in the gastric vein also showed an immediate and sharp increase following xenopsin administration. Xenopsin appeared more potent inducer of the glucagon. It is concluded that xenopsin acts directly on endocrine pancreas and gastric antrum to secrete their hormones.

Animals↗
PubMed1978

Potential endocrine effects of hypothalamic peptide "neurotensin" on pancreas in dogs.

Effects of synthetic neurotensin on the endocrine pancreas were studied in nine normal and six hypophysectomized (10th to 14th day post-hypophysectomy) dogs. Synthetic neurotensin was administered into the superior pancreaticoduodenal artery, and plasma insulin and glucagon concentrations were measured radioimmunologically. In normal dogs, ten microgram/kg neurotensin administration brought about a mild hyperglycemic response and sharp and rapid increase of plasma insulin and glucagon concentrations in the superior pancreaticoduodenal vein. A biphasic insulin response was noted in the pancreatic vein. The results suggest that a large dose of neurotensin acts directly on the endocrine pancreas causing secretion of these hormones. In hypophysectomized dogs, basal levels of plasma insulin and glucagon were decreased and neurotensin had little effect on the endocrine pancreas even with the administration of a large dose.

Animals↗
PubMed1977

Successful immunosuppressive therapy in insulin resistant diabetes caused by anti-insulin receptor autoantibodies.

A 45-year-old, non-obese female patient with no previous history of insulin administration was found to have extreme insulin resistance and abnormally high plasma immunoreactive insulin in the absence of anti-insulin antibodies in the serum. Clinically, there was no ketonuria. The patient also had evidence of Sjogren's syndrome with several immunologic features including hypergammaglobulinemia, positive antinuclear antibodies, accelerated erythrocyte sedimentation rate and leukopenia. Plasma pancreatic glucagon and C-peptide were elevated, but other endocrinologic abnormalties were not present. In this patient the insulin resistance appeared to be due to anti-insulin receptor antibodies which could be detected even in 1:500 dilution of serum. Immunosuppressive therapy with prednisolone and cyclophosphamide resulted in a decreased level of serum gamma globulin and a concomitant decrease of blood glucose level. After immunosuppressive therapy for eight months, the diabetic syndrome disappeared completely and anti-receptor antibodies in the serum were no longer detectable. Furthermore, insulin sensitivity returned to normal. However, the patient's glucose tolerance deteriorated after the temporary termination of cyclophosphamide treatment and the lowering of prednisolone dosage.

Autoantibodies↗
PubMed1976

Direct inhibitions of basal and arginine-induced plasma gastrin secretion by somatostatin in anesthetized dogs.

Effect of somatostatin on plasma gastrin levels was investigated in anesthetized dogs. Somatostatin was infused into the right gastroepiploic artery and plasma gastrin levels in the right gastroepiploic, superior pancreaticoduodenal and peripheral veins were measured by radioimmnuoassay. Somatostatin suppressed basal gastrin level promptly in the right gastroepiploic vein and impaired the normal gastrin secretion in response to intravenous infusion of arginine. The inhibitory effect of somatostatin on the plasma gastrin secretion was quite clearly demonstrated in the right gastroepiploic vein. It appears likely that the inhibition of gastrin secretion by somatostatin resulted in direct action on the gastrin secretory cell.

Animals↗
PubMed1975

[Serum immunoreactive insulin after the oral administration of single dose of tolbutamide. I. Peripheral vein immunoreactive insulin in normal subjects and mild diabetics (author's transl)].

It has been confirmed in numerous studies that the hypoglycemic effect of sulfonyl-ureas is mainly owing to its insulinogenic action. Intravenous administrations of the drugs have been adopted in many of these studies. But the oral administrations of the drugs in a few studies lead to conflicting results concerning its insulinogenic action. In this study, the concentrations of blood glucose, serum immunoreactive insulin (IRI), serum free fatty acid (FFA) and serum tolbutamide were measured following the oral administration of single dose of tolbutamide in six normal and eleven maturity onset mild diabetic subjects. The same parameters were measured after the oral administration of tolbutamide plus sodium bicarbonate in six normal subjects. The changes of these parameters were compared with the changes following the intravenous administration of sodium tolbutamide in six normal subjects. The oral administration of three grams of tolbutamide alone caused a gradual but significant decrease of blood glucose level. Serum FFA response showed an initial decrease, followed by a rebound elevation. In spite of 21 per cent reduction of blood glucose level, serum IRI level did not show any significant change throughout the observation for five hours. Serum tolbutamide concentration rose gradually and reached to 24.4+/-3.9 mg per 100 ml (Mean+/-SEM) at the end of the observation. Almost identical results were obtained in diabetic subjects. Three grams of tolbutamide plus the same dose of sodium bicarbonate were administered orally to the normal subjects. A profound decrease of blood glucose level with a nadir (35 per cent reduction) at 45 minutes and a significant increase of serum IRI level with a peak (273 per cent increase) at 20 minutes were obtained, and associated with a comparatively rapid elevation of serum tolbutamide concentration reached to 31.9+/-3.3 mg per 100 ml after three hours. From these results, it is suggested that slow rise of serum tolbutamide concentration after the oral administration of tolbutamide alone might lead to moderate secretion of insulin and sooner rise might evoke larger secretion into the pancreatic vein, and that an existence of moderate hyperinsulinism in the pancreatic venous blood after the oral administration of tolbutamide alone might cause a decrease of gluconeogenesis in the liver. And the failure of serum IRI response in the peripheral blood in spite of hyperinsulinism in the pancreatic vein might be due to hepatic trapping of the secreted insulin.

Administration, Oral↗
PubMed1975

[Serum immunoreactive insulin after the oral administration of single dose of tolbutamide. II. Pancreatic vein immunoreactive insulin in dogs (author's transl)].

The mode of action of sulfonylureas as hypoglycemic agent is not clarified yet. But it has been said in general to act by increasing the secretion of insulin from the beta cells. While, some believe that their effect is independent on insulin secretion. In the previous report, it was demonstrated that the oral administration of single dose of tolbutamide failed to increase immunoreactive insulin (IRI) in the peripheral vein in spite of significant decrease of blood glucose and free fatty acid levels both in normal and diabetic subjects. In order to observe changes of IRI level in the pancreatic vein following the oral administration of single dose of tolbutamide, the present study was carried out to determine serum IRI level of the pancreatic and peripheral vein in dogs. Mongrel dogs of both sexes, weighing 7-12 kg were anesthetized with sodium pentobarbital. A catheter was inserted into the superior pancreatico-duodenal vein through its duodenal branch after a laparotomy. Another catheter was inserted into the femoral vein for the collection of peripheral venous blood. The experiment was started one hour after the operation. Blood glucose level decreased gradually to 39 per cent reduction of the previous level at 180 minutes after intragastric administration of single dose of tolbutamide (0.1 g per kg). Serum IRI level in the peripheral vein showed only slight increase, similar to the response in man. While, pancreatic vein IRI level increased gradually and showed a fourfold increment after 180 minutes (from 143 muU per ml to 556 muU per ml), associated with a constant elevation of plasma tolbutamide concentration which showed 6.4 mg per 100 ml after 180 minutes. Simultaneous administration of 0.1 g per kg of tolbutamide and the same dose of sodium bicarbonate caused 49 per cent reduction of blood glucose level and a doubling of the basal IRI level in the peripheral vein. Serum IRI level in the pancreatic vein rose sharply and demonstrated a peak at 90 minutes (620 per cent increase). The elevation of plasma tolbutamide concentration was somewhat more rapid than that after tolbutamide alone. From these observations, it was confirmed that an apparent secretion of insulin into the pancreatic vein was induced by the oral administration of tolbutamide alone, in spite of the lack of increase in the peripheral vein IRI. And it is emphasized that the changes of insulin level in the pancreatic vein should be taken into account in a study of insulin dynamics.

Administration, Oral↗