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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 469 records · Page 26Linked to original sources
PubMed1976

Retina, tear and serum beta-N-acetylglucosaminidase activities in diabetic patients.

In previous studies, beta-N-acetyglucosaminidase activities were found to be markedly decreased in streptozotocin diabetic rat kidney, while that of the liver, spleen and intestine remained unchanged. The decrease in total kidney enzyme activity was in parallel with a decrease in the enzyme activity of the main isozyme of beta-N-acetylglucosaminidase, of which little or none was contained in the other three tissues. The present paper reports that the retina, also sensitive to diabetic microangiopathy, showed a similar isozyme pattern to that of kidney, composed of mainly type II isoenzyme of beta-N-acetylglucosaminidase. Type II isoenzyme was not detectable in any of the other materials tested including human and rat erythrocytes, lymphocytes and platelets, and human buccal epithelia and saliva, except human tear. The physiologic significance of the human tear beta-N-acetylglucosaminidase is unknown, but this enzyme was found to contain a considerable amount of Type II isoenzyme, and the enzyme activities were decreased in poorly controlled diabetic patients. Patients with retinopathy also showed markedly lowered tear enzyme activity. The diabetic patients were followed up for several months with occasional ophthalmoscopic examination and determination of serum beta-N-acetylglucosaminidase activity. As a result, changes in the latter were found to be useful as an indicator of the development of microangiopathy.

Acetylglucosaminidase↗
PubMed1976

Beta-glycosidases and diabetic microangiopathy. I. Decreases of beta-glycosidase activities in diabetic rat kidney.

Deposition of PAS2-positive materials and thickening of the basement membrane in vascular lesions are characteristic findings in diabetes mellitus, suggesting altered metabolism of glycoprotein. Changes in the activities of the glycosidases, beta-N-acetylglucosaminidase [EC 3.2.1.30], beta-glucuronidase [EC 3.2.1.31], beta-galactosidase [EC 3.2.1.23], and beta-glucosidase [EC 3.2.1.21] were measured in various organs and the serum of diabetic rats. The activities of the first three enzymes listed above were found to be much reduced in the kidney but increased in the serum. The decreased activities of beta-glycosidases in the kidney may be one of the factors responsible for the pathogenesis of microangiopathy.

Acetylglucosaminidase↗
PubMed1976

Beta-glycosidases and diabetic microangiopathy. II. An insulin-dependent isozyme of beta-N-acetylglucosaminidase.

Previously we reported that beta-glycosidase activities were markedly decreased in the kidney but increased in the serum of diabetic rats. To examine these changes, the isozymes of beta-N-acetylglucosaminidase [EC 3.2.1.30] of rats were examined by DEAE-cellulose column chromatography. At least 3 major isozymes were found in both the kidney and liver. The main isozyme was type II isozyme in normal rat kidney and type III in normal rat liver. The activity of the type II isozyme in the kidney was markedly lowered when the total activity was decreased in diabetes and its normal activity was restored on insulin treatment, in parallel with increase in the total activity in diabetes. No significant change was found in the chromatographic pattern of isozymes in the liver in diabetes. In diabetic rat serum, the increase of total activity was found to be due to increase of type I and II isozymes.

Acetylglucosaminidase↗
PubMed1976

Comparison of the changes in plasma human growth hormone (HGH) and immuno-reactive glucagon (IRG) after intravenous and subcutaneous injection of glucagon.

Ten healthy male volunteers were studied to compare the effectiveness of intravenous and subcutaneous injections of 1 mg of glucagon on HG secretion. Plasma HGH level rose to a peak of 6 ng/ml or greater 120 minutes after the subcutaneous injection of glucagon (sc glucagon) in all subjects, whereas the intravenous injection of glucagon (iv glucagon) caused comparable increments in plasma HGH in only six out of ten subjects. Furthermore, in comparison to those in sc glucagon the periods required to show maximum responses were less consistent in iv glucagon. Plasma IRG levels reached a peak of 102.4+/-22.6 ng/ml at two minutes following iv glucagon, and a peak of 3.33+/-1.08 ng/ml at 15 minutes following sc glucagon. These fell to initial levels at 60 minutes and at 180 minutes, respectively. There was no definite correlation either between the magnitudes of changes in plasma IRG and HGH levels or between the velocities of decrement in blood sugar and HGH responsiveness. Judging from its simplicity and reproducibility it may be concluded that sc glucagon is more suitable for a clinical provocative test of HGH release than is iv glucagon. In regards to the mechanism of glucagon-induced HGH release, neither glucagon per se nor the fall of blood sugar after hyperglycemia was assumed to play any major role. The sustained elevation of plasma IRG for a certain period might be responsible for the glucagon-induced HGH release.

Adult↗
PubMed1976

Endocrine function in a case of beta-adrenergic hyperdynamic circulatory state.

Endocrine functions were investigated in a case of "beta-adrenergic hyperdynamic circulatory state". This state was diagnosed by (1) typical symptoms of cardiac awareness, (2) physical findings (increments of pulse rate and blood pressure by changing positions or walking), (3) increase in cardiac output (5.25 l/min leads to 14.03 l/min) and decrease in circulatory time (10.8 sec leads to 5.5 sec) by isoproterenol infusion (0.02 mug/min/kg body weight), (4) rapid loss of symptoms and above findings by propranolol treatment (30 mg per os daily) and reappearance by discontinuing medication. The mechanism of insulin response to glucose has been a controversy as to whether the secretion is transmitted by beta-receptor or independent glucose receptor. And in this physiologic beta-adrenergic state, it was found that insulin responses in IVGTT and OGTT were within normal limit. When beta-adrenergic condition was corrected by propranolol treatment, insulin responses were shown lowered, though in the normal range. This could be reproduced by discontinuing medication. Insulin, glucagon and growth hormone secretions caused by arginine were also found normal, but during the period the patient was on propranolol therapy, all responses were decreased, within the normal range. These results do not positively support the idea that glucose receptor is linked to beta-receptor. They do not either agree with the contention that secretions of insulin, glucagon and growth hormone induced by arginine are mediated through beta-receptors.

Arginine↗
PubMed1976

The pancreatic alpha and beta cells responses to 1-arginine and insulin-induced hypoglycaemia in hyperthyroidism.

In order to assess the secretory capacity of the pancreatic alpha and beta cells in patients with hyperthyroidism, the plasma glucagon and insulin responses to 1-arginine and insulin-induced hypoglycaemia in 12 patients were compared with those in 6 normal subjects. The response of beta cell to hypoglycaemia was evaluated by measuring the decrease in plasma C-peptide immunoreactivity (CPR) level. There was a negligible rise in blood glucose and plasma insulin levels in the patients, whereas a significant increase occurred in normal subjects during the arginine infusion. Although no difference in the fasting plasma glucagon concentration between the two groups was found, 30 min after the beginning of the arginine infusion, the plasma glucagon levels rose to a peak of 252 +/- 35 pg/ml in the patients, a value significantly lower than 387 +/- 53 pg/ml in the normal subjects. The insulin-induced hypoglycaemia caused no significant difference in the peak values of plasma glucagon between the two groups. There was a sigificant difference in the peak values of plasma glucagon between the two groups; There was a significant fall in plasma CPR after the insulin injection in both groups but the per cent decrement was rather greater in the patients than in the normal subjects.

Adolescent↗
PubMed1975

Effect of an exposure to chloramine-T on the immunoreactivity of glucagon.

Various preparations of glucagon treated with chloramine-T under different conditions have been studied with respect to their immunoreactivity toward two different glucagon antisera; one specific for pancreatic glucagon and the other capable of reacting with enteroglucagon as well. The glucagon preparations exposed to chloramine-T for different periods reacted almost identically with the nonspecific antibody whether they were used as tracer or standard. On the contrary, treatment with chloramine-T under severe conditions led to reduced immunoreactivity toward the specific antibody. Inclusion of dimethyl sulfoxide (DMSO) in the chloramine-T reaction resulted in preservation of the immunoreactivity of the treated preparations. The cyanogen bromide cleaved-glucagon, (1-26) homoserine lactone, showed little cross-reactivity with the specific antibody whereas it reacted to a similar extent with the nonspecific antibody as natural glucagon did. Amino acid analysis of the hormone exposed to chloramine-T demonstrated that the methionine residue at position 27 in the glucagon molecule had been oxidized to methionine sulfoxide. In addition, tryptophan had also been affected. DMSO protected methionine and tryptophan from the oxidative action of chloramine-T. We postulate from these results that the change in the immunoreactivity toward the specific antibody of glucagon exposed to chloramine-T is mainly due to oxidation of the methionine residue at position 27 in the molecule. The usefulness of DMSO in the iodination process is also discussed.

Animals↗
PubMed1975

Dietary therapy and insulin secretory response to glucose in adult-onset non-obese diabetic subjects.

The effect of a 4-week diet regulation on non-obese, adul-onset diabetics was studied. The diet, which was prescribed for them, was composed of 60% carbohydrate, 15-20% protein and 20-25% fat. The total caloric intake was restricted to 30, 35 and 40 Cal/kg ideal body weight depending on their physical activity. In the group whose calculated diet showed over 10% reduction in total caloric intake and carbohydrate intake, fasting glucose was decreased and glucose tolerance was improved significantly after the 4-week dietary therapy. Insulin response to oral glucose loading was improved, particularly in the later stage of oral glucose tolerance test. As a result, insulin area, i. e. the total area under the insulin curve was increased to almost two times. The sensitivity to insulin did not show any significant changes after diet regulation. The present data indicate that the therapeutic effect of the diet restriction should be at least in part ascribed to the increased secretion of insulin. In the treatment of diabetics, a restricted diet is essential and beneficial from the point of view that it could improve the pancreatic beta-cell function.

Adult↗
PubMed1975

Boiling method for the extraction of gut glucagon-like immunoreactive materials.

The boiling method deviced in accordance with the extraction procedure of secretin was applied to the extraction of gut glucagon-like immunoreactive material (GLI) and compared with the acid alcohol method of Kenny with respect to efficiency of the extraction and property of the extracted materials. GLI was extracted from minced porcine small intestine by each method. The total amount of GLI extracted by the boiling method was 14.45+/-2.07 mug/10g small intestine (mean+/-SE), showing a high yield as compared to 4.07+/-0.29 mug/10 g small intestine obtained by the acid alcohol method. The difference was statistically significant (p less than 0.005). The gel chromatogram of the acid alcohol extract was separated into two peaks; peak 1 appeared before the the insulin marker, while peak II was eluted with the glucagon marker. The chromatogram of the boiling extract has a main broad fraction including insulin marker and a minor second peak corresponding to peak II of the acid alcohol extract. Boiling of the acid alcohol extract did not cause any shift of peak I in chromatogram. GLI present in the first half of the main fraction of the boiling extract was different from that in the latter half, but identical to peak I of the acid alcohol extract with respect to the immunoreactivity against glucagon antibody. It is concluded that in the extraction of GLI not only high yield is achieved but one or more new components is picked up by the boiling procedure as compared to the acid alcohol method.

Animals↗
PubMed1975

Effect of phenformin on the response of plasma intestinal glucagon-like immunoreactivity (GLI) to oral glucose in gastrectomized subjects.

The effect of phenformin (DBI) on the plasma intestinal glucagon-like immunoreactivity (GLI) and pancreatic glucagon (IRG) responses to oral and intravenous glucose loads were studied in 26 gastrectomized subjects, using a cross-reacting and an IRG-specific anti-serum. The drug produced no significant changes in fasting GLI and IRG levels. Thirty minutes after oral glucose alone, the total GLI level rose to a peak of 1.55 +/- 0.17 ng/ml in the untreated subjects and to a maximum level of 1.67 +/- 0.18 ng/ml in the DBI-pretreated subjects. However, the mean GLI levels obtained 120 and 180 min after oral glucose were significantly higher after treatment with DBI. The blood sugar and IRI responses to oral glucose were lowered significantly by DBI pretreatment. DBI did not alter the glucose, IRI, IRG and GLI response to intravenous glucose. These results suggest that the release of intestinal GLI is not related to the intestinal absorption of glucose.

Adult↗