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K Horigome

Publications and source records attributed to K Horigome.

At least 37 records · Page 2Linked to original sources
PubMed1987

Amino acid composition and NH2-terminal amino acid sequence of rat platelet secretory phospholipase A2.

The amino acid composition and partial NH2-terminal amino acid sequence of the phospholipase A2 secreted by stimulated rat platelets were determined. The most predominant amino acid in the phospholipase A2 was cysteine followed by lysine, suggesting that it is a basic one. This finding is consistent with its high affinity to a cation exchange column. The NH2-terminal 24 amino acids were found to be as follows: X-Leu-Leu-Glu-Phe-Gly-Gln-Met-Ile-Leu-Phe-Lys-Thr-Gly-Lys-Arg-Ala-Asp- Val-Ser-Tyr-Gly-Phe-Tyr-Gly- The enzymes contains 5Phe, 8Met, 9Ile, 24Tyr, and 25Gly residues, all of which are conserved in the sequenced pancreatic phospholipase A2. This is the first report of the tentative characterization of a eukaryotic phospholipase A2, the cellular source of which is known, i.e., it does not originate from a venom or the pancreas.

Amino Acid Sequence↗
PubMed1986

Effect of serine phospholipid structure on the enhancement of concanavalin A-induced degranulation in rat mast cells.

The correlations among the potentiating activity of various PS analogs on concanavalin A (Con A)-induced rat mast cell degranulation, the hemolytic activity and the incorporation into the mast cell membrane were studied. The following results were obtained. Lysophosphatidylserine (LysoPS) caused rat mast cell activation (degranulation) in the presence of Con A. The order of the activity was as follows: 1-stearoyl lysoPS = 1-palmitoyl lysoPS greater than 1-myristoyl lysoPS greater than 1-lauroyl lysoPS. The relative hemolytic activity of these compounds was similar to that observed in the mast cell activation. Dilauroyl PS, which shows similar hemolytic activity to 1-myristoyl lysoPS, did not activate mast cells appreciably. The relative activity of these phospholipids in the binding to mast cells was 1-stearoyl lysoPS greater than dilauroyl PS greater than 1-lauroyl lysoPS. Hemolytic activity, as well as activity on mast cells, of lysoPS analogs was well correlated to mast cell membrane incorporation, whereas such a correlation was not found with PS analogs. Dilauroyl PS could be accumulated in the mast cell membrane and showed hemolytic activity, but did not activate histamine secretion.

Animals↗
PubMed1986

Metabolism of lysophosphatidylserine, a potentiator of histamine release in rat mast cells.

Lysophosphatidylserine (lysoPS) strongly enhances degranulation of rat mast cells induced by concanavalin A (Con A). In the present paper, the metabolism of exogenous lysoPS in intact mast cells was investigated. Incubation of mast cells with 1-stearoyl-sn-glycero-3-phospho-[3-3H]serine resulted in the rapid binding of lysoPS to mast cells and the time-dependent formation of a considerable amount of [3H]phosphatidylserine. No other radiolabeled lipid metabolites were detected. These results suggest that phosphatidylserine (PS) is synthesized through acylation of lysoPS incorporated into mast cells. Most of the lysoPS associated with mast cells was removed by washing with bovine serum albumin, whereas PS newly formed from lysoPS was not. The cells washed with albumin showed no appreciable histamine release upon subsequent addition of Con A. A different set of experiments was performed using lysoPS analogs which were modified at the hydroxyl group at position 2 of glycerol to avoid acylation. 1-Stearoyl-2-O-methyl-glycero-3-phosphoserine showed almost the same potentiating activity as 1-stearoyl-lysoPS, although the former does not have the free hydroxyl moiety at position 2 of the glycerol residue. The enhancing activity of another lysoPS analog, 1-stearyl-propanediol-3-phosphoserine, which lacks the hydroxyl group altogether, was quite similar to that of 1-stearyl-lysoPS. From these results we conclude that the acylation of lysoPS bears no relation to its potentiating activity and that lysoPS acts toward mast cells as lysoPS itself without any conversion to PS. The effect of replacement of an ester bond at position 1 of glycerol in lysoPS with an ether bond, and the phospholipid composition of rat mast cells are also discussed.

Animals↗
PubMed1984

Production of cholera-like enterotoxin by Aeromonas hydrophila.

A total of 249 strains of mesophilic Aeromonas including 179 A. hydrophila and 70 A. caviae were tested for production of cholera-like enterotoxin by reversed passive latex agglutination (RPLA) assay. A cholera-like enterotoxin neutralized with cholera antitoxin was demonstrated in the culture filtrates from eight (4.5%) of the 179 A. hydrophila strains, while none of A. caviae strains revealed the enterotoxin production in the test. Production of the cholera-like enterotoxin in the eight strains of A. hydrophila was also confirmed by enzyme-linked immunosorbent assay (ELISA).

Aeromonas↗
PubMed1983

[Clinical efficacy of cefotaxime in the field of internal medicine].

Fifty-eight patients were treated with cefotaxime (CTX, Claforan) intravenously. Almost all patients (54 patients) had underlying diseases that were 16 cases of diabetes mellitus, 10 cases of respiratory diseases, 8 cases of cerebral vascular disturbance, 6 cases of renal diseases and blood diseases, 5 cases of carcinoma and hypertension, 4 cases of cholelithiasis, 3 cases of heart diseases and 7 cases of other diseases. The clinical efficacy of CTX in 34 cases of RTI, 11 cases of UTI, 8 cases of BTI and 5 cases of other infection was excellent in 11 cases, good in 27 cases, fair in 12 cases, poor in 4 cases and unclear in 4 cases. The over all clinical effectiveness was 70.4%. No adverse reaction was observed except for 2 cases (general fatigue in 1 case and eruption and itching in another). These results obtained should support the usefulness of CTX.

Adult↗
PubMed1978

Effect of caerulein upon insulin and glucagon secretion in dogs.

In order to investigate the action of caerulein upon insulin and glucagon secretion, experimental studies were carried out using anesthetized dogs, in which graded doses of caerulein were infused into the pancreatic artery, and insulin and glucagon were measured in the blood obtained from the pancreatic vein. When caerulein was administered at a rate of 15 ng/min, neigher changes of blood glucose in the femoral artery nor plasma levels of insulin or glucagon in the pancreatic vein were prominent. Caerulein infusion at a rate of 120, 240 or 480 ng/min caused a prompt rise of plasma insulin and a delayed increase of plasma glucagon in the pancreatin vein. Blood glucose in the femoral artery increased only with caerulein doses of 240 ng/min or more. A significant increase in pancreatic vein blood flow rate was demonstrated after the infusion of caerulein at a rate of 240 ng/min or more. Neither caerulein-induced insulin secretion nor glucagon secretion was influenced by a simultaneous infusion of glucose. In contrast, caerulein-induced glucagon secretion was exaggreated by a simultaneous arginine infusion. It was concluded from the present experiments that caerulein infusion into the pancreatic artery resulted in increased secretion of insulin and glucagon from the pancreas.

Animals↗
PubMed1978

Abnormal response of pancreatic glucagon to glycemic changes in diabetes mellitus.

In order to determine pancreatic alpha cell function in diabetes mellitus, plasma glucagon responses to either an oral glucose load or insulin-induced hypoglycemia were investigated. Plasma glucagon in 6 normal control subjects fell significantly after the administration of glucose, whereas the levels of plasma glucagon did not decrease after glucose ingestion in patients with diabetes mellitus. In the group with severe diabetes, whose fasting blood glucose exceeded 200 mg/100 ml, the plasma glucagon level rose after glucose administration instead of decreasing. In 6 patients with diabetes mellitus, plasma glucagon did not decrease but rather increased during a glucose tolerance test which was performed after treatment with insulin and/or diet. In 6 control subjects, there was a remarkable rise of plasma glucagon in response to insulin-induced hypoglycemia. In contrast, no significant rise in plasma glucagon was demonstrated in 19 diabetic subjects undergoing intravenous insulin test. Seven patients, in whom an insulin test was repeated after treatment with insulin, sulfonylurea, or diet had a small rise in peak plasma glucagon and an increase in the integrated area under the glucagon response curve. It is concluded that the abnormal glucagon response to changes in blood glucose might be a primary defect in diabetes mellitus.

Adult↗
PubMed1977

Heterogeneity of extractable gut glucagon-like immunoreactivity (GLI) and its lipolytic activity.

Gut glucagon-like immunoreactivity (GLI) was extracted from the mucosa of the canine intestine and was separated into two peaks by gel filtration; Peak I (7,000 daltons) and Peak II (3,500 daltons). These two peaks were purified by means of affinity chromatography using an anti-glucagon antibody as a ligand substance. These purified gut GLIs were not composed of single component, when applied to ion exchange chromatography. These partially purified Peak I and Peak II showed lipolytic activities, though very weak in potency, in vitro on the rat fat tissue at pharmacologically high concentration (5 ng eq/ml in final). It was concluded that gut GLI, even though purified, showed heterogeneity and that gut GLI revealed lipolytic activity although weak in potency compared with pancreatic glucagon.

Adipose Tissue↗
PubMed1977

Insulin response to glucose or glucagon in subclinical diabetes previously injected with tolbutamide.

Thirty-one patients with subclinical diabetes, who showed diabetic or impaired glucose tolerance after treatment for diabetes, were investigated in order to clarify the abnormalities of insulin response in diabetes mellitus. These patients showed a delayed response of plasma insulin during oral glucose loading. In the tolbutamide-glucose test, in which glucose loading followed the intravenous tolbutamide injection at a 60-min interval, the insulin level at 90 min was significantly lowered in a group of 20 patients with subclinical diabetes. In the tolbutamide-glucagon test, in which 1 mg of glucagon was injected 60 min after tolbutamide injection, the maximal level of plasma insulin was significantly decreased in a group of 10 subclinical diabetes except for one patient. These results indicate that insulinogenesis and/or release of insulin were decreased even in subclinical diabetes, suggesting that such a defect in islet function might be one of the abnormalities in primary diabetes.

Blood Glucose↗
PubMed1977

Changes in glucose tolerance and insulin response in subclinical diabetes after treatment.

In this study, 121 patients who showed diabetic or decreased glucose tolerance and were treated with diet alone for one to fifteen years were investigated as subclinical diabetes. Glucose tolerance in these patients was improved or remained unchanged during the clinical course. Aggravation in glucose tolerance was observed in only seven cases. However, abnormalities in glucose tolerance were still found in 107 cases (88%) of the subclinical diabetes. Insulin response to oral glucose was investigated in 74 patients with subclinical diabetes. Delayed response and/or decreased response in the initial phase were demonstrated in 58 out of 74 patients (79%). No significant difference was observed in the insulinogenic index (ratio of insulin increment/glucose increment) at 30 min between the normal controls and either group with abnormal glucose tolerance. Diabetic retinopathy, including microaneurysm, was detected in 25 out of 109 patients with diabetic glucose tolerance. Abnormal insulin response, delayed and/or decreased, was demonstrated in 13 of 16 patients with diabetic retinopathy (81%). These results indicate the possibility that subclinical diabetes in the present study is a mild type of primary diabetes. In addition, it is suggested that abnormal response of plasma insulin to glucose, delayed and/or decreased, might be one of the prominent findings in diagnosis of diabetes mellitus.

Adult↗
PubMed1976

Purification of canine gut glucagon-like immunoreactivity (GLI) and its insulin releasing activity.

In order to clarify the nature of the biological action of gut glucagon-like immunoreactivity (GLI), GLI was extracted from the mucosa of the canine intestine and purified by gel filtration and affinity chromatography. 1500 gm of the mucosa yielded approximately 7 gm of crude extract of GLI. This crude extract was applied to a column packed with Sephadex G-50 or Bio-Gel P-10 and two peaks were obtained, Peak I and II. Each peak was purified with affinity chromatography, bound to gamma-globulin of anti-glucagon rabbit-serum. In this step, the GLI was purified approximately 80 times in comparison with the crude extract. Peak I or Peak II, as well as pancreatic glucagon, was infused successively into the pancreaticoduodenal artery of the anesthetized dogs. When buffer solution or the Peak I GLI was infused, the plasma immunoreactive insulin in the pancreatic vein did not change significantly. In contrast, both the Peak II and pancreatic glucagon promoted insulin secretion from the pancreas. The results obtained in this experiment demonstrate the promotion of insulin release from the pancreas and suggest an important role of gut GLI in the absorption and metabolic processing of nutrients.

Animals↗
PubMed1976

Insulin and glucagon response in patients with chronic pancreatitis.

The oral glucose tolerance test and arginine infusion test were carried out on 22 patients with chronic pancreatitis and 11 normal control subjects. According to the glucose tolerance curve, the patients were divided into three groups; group I (normal or slightly impaired), group II (mildly diabetic) and group III (moderately diabetic). Markedly impaired insulin responses to oral glucose as well as to arginine infusion were observed in groups II and III. In group I, the mean plasma insulin levels during glucose tolerance test were the same as those in the controls, but the insulin response to arginine was reduced except in two cases. On the other hand, the glucagon levels during arginine infusion test were within the normal range in group I and slightly reduced in the other groups with diabetic glucose tolerance. The ratio of increment area of insulin to that of glucagon during arginine infusion in the patients was slightly decreased in comparison with the controls. Neither insulin nor glucagon response after arginine infusion showed a significant correlation with pancreatic exocrine function. It is concluded that in chronic pancreatitis insulin response to glucose as well as to arginine is markedly decreased, and that glucagon rise after arginine infusion is lowered compared with the controls.

Adolescent↗
PubMed1975

Plasma glucagon-like immunoreactivity (GLI) in dogs.

Gut glucagon-like immunoreactivity (GLI) was extracted from plasma of dogs and was compared for its molecular size and insulin releasing activity with GLI present in the intestine. Plasma was obtained from the portal vein of dogs, of which the pancreas was removed as rapidly as possible during the glucose administration into the intestine. Plasma GLI of intestinal origin was extracted by a modification of Kenny's method. The amount of GLI extractable from plasma in each dog ranged from 4.30 to 25.74 ng. The extract of plasma during glucose absorption was observed to have two peaks on gel filtration, corresponding to Peak I and Peak II of GLI extracted from the gastrointestinal tract. The intrapancreatic infusion of the Peak II GLI extractable from plasma promoted remarkable insulin release in dogs, like pancreatic glucagon. In contrast, the Peak I GLI from plasma caused an equivocal rise of insulin in the pancreatic vein. It is concluded from the experiment that gut GLI extracted from plasma shows the same elution pattern on gel filtration and the same insulin releasing activity as GLI extractable from the gut.

Animals↗
PubMed1975

Diagnostic value of intravenous glucagon test in insulinoma.

The intravenous glucagon test was performed in 11 patients with insulinoma and the diagnostic significance of the test was studied in comparison with the glucose test, the tolbutamide test and the arginine test. The curves of plasma insulin following the intravenous administration of glucagon were markedly different and strange in those patients with insulinoma compared with the normal controls. The maximal levels of plasma insulin ranged from 85 to 400 muU/ml, exceeding the normal range in 10 out of 11 patients, or 91%. Increased levels in the maximal plasma insulin were observed in 63%, 100% and 56% through the glucose test, the tolbutamide test and the arginine test, respectively. The distribution of the insulin areas, calculated from the insulin curves during these tests, was shown to be similar to that of the maximal levels of plasma insulin. There was no significant correlations between the maximal levels of plasma insulin in the glucagon test and the glucose test, the tolbutamide test or the arginine test. The present experiment demonstrated that the intravenous glucagon test, next to the tolbutamide test, caused a large increase in plasma insulin, and therefore, that this test is one of the most useful tools among the provocation tests, for the diagnosis of insulinoma.

Adenoma, Islet Cell↗