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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 451 records · Page 25Linked to original sources
PubMed1979

Anomeric specificity in the response of gut glucagon-like immunoreactive materials to glucose.

An anomeric specificity of the glucose sensors of A cells and B cells of the pancreas has been reported. In this context the present authors investigated, using the canine intestinal loop prepared from the terminal portion of the ileum, how glucagon-like immunoreactive materials (GLI) of the gut would respond to glucose anomers in an attempt to explore a possible anomeric specificity of glucose-stimulated gut GLI secretion. As a result GLI was found to be more readily released into the blood stream after an intestinal alpha-glucose load than following beta-gluocse during a 15-minute observation period. It is thus suggested that gut GLI-secreting cells have glucose sensors similar to those of pancreatic A or B cells which are specific for the alpha-glucose anomer.

Animals↗
PubMed1979

Half life of gastrointestinal glucagon-like immunoreactive materials.

The composition, half life and hyperglycemic action of the porcine gastrointestinal glucagon-like immunoreactive materials were examined. Glucagon immunoreactivity (GI) measured using specific antiglucagon serum was more abundunt in the extract from the gastric fundus than in the one from the small intestine. When the extract from the gastric fundus was injected in dogs, the half life (T1/2) of total glucagon-like immunoreactivity (total GLI) measured using nonspecific antiglucagon serum was 9.5 +/- 1.1 min (mean +/- SEM), which was longer than that of crystalline pancreatic glucagon, 3.4 +/- 0.2 min, but shorter than that of the extract from the small intestine, 15.9 +/- 1.3 min. On the other hand, T1/2 for GI from the gastric fundus was 5.1 +/- 0.9 min, which was not significantly different from that of crystalline pancreatic glucagon. Blood sugar levels were significantly increased from the basal by 25 +/- 4 mg/100 ml at 10 min and 19 +/- 4 mg/100 ml at 15 min following an injection of the extract from the gastric fundus, but such a change in blood sugar levels was not demonstrated when the extract from the small intestine was injected. These results suggest that GI of the gastric fundus is close to pancreatic glucagon in respect of its metabolism and hyperglycemic activity.

Animals↗
PubMed1979

A-Cell and gut glucagon in normal and depancreatized dogs. Inhibition by somatostatin and insulin.

The effect of somatostatin (SRIF) and of insulin on the plasma levels of immunoreactive glucagon (IRG) and glucose was examined in normal (N) and depancreatized (PX) dogs. The infusion of SRIF (3 microgram/min for 15 min) caused a rapid decrease of the total IRG measured by means of an antiglucanon serum (AGS 10) which cross reacts with extracts of intestinal mucosa. This decrease was due primarily to a fall in the IRG fraction measured by an antiserum (AGS 18) specific for the carboxyl terminus of pancreatic or A-cell IRG. When the dose of SRIF was increased to 10 microgram/min for 90 min, the difference between total and A-cell IRG in the systemic blood also decreased, indicating that other IRG fractions, such as gut IRG, had also been suppressed. The introduction of 50 ml of a 5% glucose solution into a loop of ileum was followed by an increase of gut IRG measured in the regional mesenteric blood. This response was suppressed by the infusion of SRIF (3 microgram/min). Insulin suppressed the basal level of total IRG, but did not alter the gut IRG response to glucose. The SRIF- and insulin-induced reduction in plasma IRG was not associated with a reduction in plasma glucose, suggesting that the high levels of total and A-cell IRG observed in depancreatized dogs were not essential for the maintenance of hyperglycemia.

Animals↗
PubMed1978

[Glucagon-releasing activity of xenopsin, neurotensin and substance P in the perfused rat pancreas (author's transl)].

It has been reported that Xenopsin, Neurotensin and Substance P change plasma glucagon and insulin levels when they are administered in vivo. In order to clarify whether these agents have a direct effect on glucagon and insulin secretion from the pancreas, the action of each substance was examined by using the rat pancreas perfusion technique. The results were as follows: The perfusion with 1 and 5 nmole/min of Xenopsin for ten minutes resulted in a significant but transient release within two minutes. Neurotensin did not show any stimulatory effect on glucagon release in the concentration of 1 or 5 nmole/min for ten minutes. However, Substance P lowered significantly the glucagon concentration in the perfusate in a similar concentration. None of these substances influenced significantly insulin release from the perfused pancreas. These findings suggest that the hyperglucagonemia caused by these three agents in vivo may not be attributed to the direct effect on the pancreatic A-cell.

Animals↗
PubMed1978

Lack of gastrointestinal glucagon response to hypoglycaemia in depancreatized dogs.

Fasting (24 h) normal dogs and depancreatized dogs were injected intravenously with highly purified porcine insulin (Actrapid) in the doses of 0.2 U/kg and 0.5 U/kg, respectively. Blood glucose decreased from 152 +/- 41 (SEM) mg/100 ml to 39 +/- 7 mg/100 ml in the depancreatized dog and from 95 +/- 3 mg/100 ml to 42 +/- 4 mg/100 ml in the normal animal. Using a specific antiserum for "pancreatic" glucagon, the circulating level of glucagon immunoreactivity did not rise from the basal value of 247 +/- 31 pg/ml in the depancreatized group whereas it rose significantly from 223 +/- 24 pg/ml to 321 +/- 41 pg/ml in the normal group. In contrast intravenous infusion of 7 g of arginine increased "pancreatic" glucagon immunoreactivity in both groups. Thus, extrapancreatic glucagon of the pancreatic type does not respond to hypoglycaemia but to arginine infusion.

Animals↗
PubMed1978

Failure of somatostatin to decrease blood glucose by suppression of extrapancreatic glucagon in severely diabetic depancreatized dogs.

Effects of somatostatin on extrapancreatic glucagon secretion in totally depancreatized dogs were examined. Somatostatin infusion at a rate of 3 microgram/min showed a rapid decrease of total glucagon-like immunoreactive materials (total GLI) measured by nonspecific antiserum, AGS 10, and gut glucagon immunoreactivity (gut GI) measured by specific antiserum, AGS 18, in systemic blood. Gut GLI calculated as the difference between total GLI and GI did not decrease significantly within 30 min. No changes of blood glucose were noted. Significant decreases of all glucagon fractions were observed when the rate of somatostatin infusion was increased to 10 microgram/min and prolonged for 90 min, whereas again blood glucose did not change at all. It is concluded that somatostatin inhibits both gut GI and GLI secretion, although gut GLI remains in circulation longer than gut GI. Suppression of gut GI is not effective for the reduction of blood glucose once an extreme hyperglycemia is brought about by insulin deficiency.

Animals↗
PubMed1977

[Aging and endocrine pancreas (author's transl)].

To test the hypothesis that diabetes is a form of accelerated aging, the following observations were made. 1) The incidence rate of diabetes mellitus had its peak at around 50 years of age with a gradually decreasing rate thereafter. This was clearly different from the manner of incidence of such disease as arteriosclerosis which increased with advancing age. 2) 100g of the oral glucose tolerance test performed on elderly subjects aged 60 to 89 years revealed high incidence of abnormal tolerance, 21% diabetic and 53% borderline types. 3) The insulin secretory capacity to glucose load of subjects was not different from that of young and middle-aged subjects from 20 to 49 years old. Therefore, decreased tolerance to glucose load could not ba ascribed to deficient insulin secretion. 4) No abnormality of glucagon response to glucose load was found in the old. 5) Serum beta-N-acetylhexosaminidase activity was not increased in elderly subjects, again contrasting with the increased activity found in diabetics. 6) Both glycolytic and gluconeogenic enzyme activities were decreased in the liver of aged rats. 7) No specific abnromality in insulin secretory response was observed in Werner's syndrome which might be considered to be a model for aging. All the above observations do not support the aforementioned hypothesis. Abnormality of glucose tolerance frequently observed in elderly subjects appears to be caused by other pathogenesis than diabetes mellitus.

Adolescent↗
PubMed1977

Failure of exogenous insulin to inhibit insulin secretion in man.

In order to explore whether or not the negative feedback mechanism of insulin per se on insulin secretion exists in man, changes in plasma C-peptide immunoreactivity (CPR), as an index of pancreatic B cells secretory function, were studied in 6 nonobese healthy volunteers in the presence of high circulating levels of exogenous insulin. 10% glucose was infused concurrently so as to maintain blood sugar at the basal level. The insulin-glucose infusion was maintained for 120 minutes, achieving mean plasma levels of 140-180 mu1/ml. After this period, the insulin infusion was continued at the same rate for an additional 10 minutes while the glucose was omitted. Despite the elevated level of circulating insulin, no significant change in plasma CPR concentration was observed so long as the blood sugar was maintained at the basal levels. Following cessation of the glucose infusion, the plasma CPR levels declined with a decrease in blood sugar level. Under the conditions of the present study, no inhibitory effect of exogenous insulin on the secretory function of the B cells was noticed.

Adult↗
PubMed1977

Enhanced endogenous insulin secretion after treatment with monocomponent insulin.

Eight maturity-onset diabetic patients who had no infections, liver diseases or other endocrine diseases which might affect carbohydrate metabolism were treated with monocomponent lente insulin, which is known to have little antigenicity, until blood sugar was controlled. The diurnal values of the blood sugar (BS) and immunoreactive insulin (IRI) were obtained before treatment and on the third day after the withdrawal of insulin treatment. One patient was dropped from the study because of insulin antibody formation. The total integrated IRI area in the diurnal profile was increased from 98.9 +/- 23.7 to 186.1 +/- 37.7 muU.h/ml (p less than 0.05), while the total blood sugar area was decreased from 7,500 +/- 1,200 to 5,510 +/- 1,214 mg-h% (p less than 0.05). Oral Glucose Tolerance Test on the fourth day after the withdrawal of insulin treatment showed increased IRI response compared to pretreatment. It is concluded that endogenous insulin secretion could be increased in the diabetic patient by the metabolic control with exogenous insulin injections.

Adult↗
PubMed1977

Insulin releasing activity of gastrointestinal glucagon-like immunoreactive materials in perfused rat pancreas.

Insulin-releasing activity of porcine gastrointestinal glucagon-like immunoreactive materials purified by affinity chromatography was examined in the perfused rat pancreas. When glucose concentration of the perfusate was raised from 60 to 100 mg/dl, augmented insulin release was observed. The mean incremental area of immunoreactive insulin (sigma delta IRI) during the first 10 min thus observed was 19.07 +/- 3.76 ng/10 min. Pancreatic glucagon and the extract from the gastric fundus showed the enhancement of insulin release in this system when they were added to the perfusate at the rate of 100 ng/min for 5 min; delta IRI were 41.92 +/- 8.47 and 71.70 +/- 18.09 ng/10 min, respectively, which were significantly higher than that of 100 mg/dl of glucose alone. However, no significant difference in the insulinogenic activity was noticed between the extracts from the small intestine and the control. These results suggest that the extract from the gastric fundus has insulinogenic activity similar to that of pancreatic glucagon.

Animals↗
PubMed1977

Mechanism of hypoglycemia observed in a patient with insulin autoimmune syndrome.

A 21-year-old female patient complaining of frequent hypoglycemic attacks in the presence of a large amount of circulating insulin-binding antibodies without previous known immunization is described. In order to clarify the possible mechanism of the hypoglycemic attacks occurring in this new syndrome, changes in plasma glucose, plasma total and free immunoreactive insulin (IRI), and C peptide immunoreactivity (CPR) levels were investigated in the patient before, during, and after a three-hour glucose infusion. The character of her antibodies were also examined. An abrupt discontinuation of the glucose infusion caused a sharp decline in the plasma glucose level, reaching a nadir of 30 mg./100 nk, at 270 minutes; then she became unconscious. A huge amount of total IRI of 2,834 micron U./ml. was registered at 180 minutes, while the peak value of free IRI of 208 micronU./ml. was observed 45 minutes after the cessation of the glucose infusion. Plasma CPR was increased from high basal level, 19.6 ng./ml., to the maximum level of 29.2 ng./ml. The maximum insulin-binding capacity of IgG in the patient's serum was 6.25 mU./ml. The antibody-combining site was homogeneous, showing one high-affinity site (K: 1.1 X 10(9)M-1). Neither the prolonged fasting nor the administration of tolbutamide induced the hypoglycemic attack in the patient. The hypoglycemia may be explained by an unduly excessive amount of insulin liberated from a large pool of bound insulin irrespective of blood sugar level. The cause of the antibody production is also discussed.

Adult↗