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S Kadowaki

Publications and source records attributed to S Kadowaki.

At least 73 records · Page 4Linked to original sources
PubMed1986

Calcitonin gene-related peptide stimulates somatostatin release from isolated perfused rat stomach.

Effect of calcitonin gene-related peptide (CGRP) on somatostatin release was investigated on the isolated perfused rat stomach. Perfusion with CGRP (0.1 nM-100 nM) caused a significant and dose-dependent increase in effluent somatostatin levels. The somatostatin response to CGRP was rapid in onset and reversible immediately after the cessation of CGRP infusion. These findings suggest that CGRP stimulates the release of gastric somatostatin, thereby modulating gastric functions in rat.

Animals↗
PubMed1986

[Effects of MY-5116 on experimental animal models of type I-type IV allergic reactions and the formation of IgE antibody].

The effects of a new anti-allergic agent, MY-5116: isoamyl 5,6-dihydro-7,8-dimethyl-4,5-dioxo-4H-pyrano [3,2-c] quinoline-2-carboxylate, on experimental animal models of type I approximately type IV allergic reactions and the formation of IgE antibody were investigated. MY-5116 administered intraperitoneally at doses of 30 and 100 mg/kg suppressed significantly the homologous PCA in guinea pigs. MY-5116 administered intraperitoneally at the dose of 100 mg/kg also suppressed significantly the heterologous PCA in guinea pigs. MY-1250, the main active metabolite of MY-5116, showed no suppression on the Schultz-Dale reaction in guinea pigs, and MY-5116 showed no inhibition on the active systemic anaphylaxis in mice (type I). MY-5116 showed no inhibition on the reversed cutaneous anaphylaxis in rats (type II), the Forssman reaction in guinea pigs (type II), the Arthus reaction in mice (type III) and the delayed type hypersensitivity in mice (type IV). MY-5116 showed no suppression on the formation of IgE antibody in C3H/He and BALB/c mice and rats. From these results, it is concluded that MY-5116 selectively suppresses the experimental models of type I allergic reaction.

Anaphylaxis↗
PubMed1986

Hb Himeji or beta 140 (H18) Ala----Asp. A slightly unstable hemoglobin with increased beta N-terminal glycation.

A fast-moving abnormal hemoglobin found in a diabetic patient was identified as beta 140 (H18) Ala----Asp. It comprised about 40% of the total hemoglobin. The beta N-terminal glycation in the abnormal hemoglobin was estimated to be 3 times as much as that in Hb A in the same blood sample. The abnormal hemoglobin was slightly unstable. Oxygen affinity of the stripped hemoglobin was decreased, but that of red cells from the carrier was slightly higher than normal because of the reduced effect of 2,3-diphosphoglycerate.

Blood Protein Electrophoresis↗
PubMed1986

Effect of 1 alpha (OH)-vitamin D3 on insulin secretion in diabetes mellitus.

Fourteen non-insulin-dependent diabetic subjects were placed on a balanced diet for 2-3 weeks followed by the same balanced diet alone (group I: control, n = 7) or daily administration of 1 alpha (OH)-vitamin D3 (1 alpha (OH)D3) (group II: 2 micrograms/day, n = 7) additionally for the next 3 weeks. A 75 g oral glucose loading test was conducted before and after the experiment and the plasma insulin response was compared along with the metabolic parameters including serum calcium, phosphorus and serum lipids. The following results were obtained. (1) Total insulin secretion in response to 75 g glucose loading was significantly increased in group II (16.3 +/- 3.9 microU/2 h/ml versus 22.7 +/- 4.9 microU/2 h/ml; P less than 0.05), though no difference was demonstrated in group I. (2) Mean serum calcium level was significantly increased from 9.4 +/- 0.1 mg/dl to 9.6 +/- 0.1 mg/dl (P less than 0.05) and serum free fatty acid level was decreased from 0.80 +/- 0.07 mEq/l to 0.53 +/- 0.07 mEq/l (P less than 0.05) in group II, but not in group I. (3) However, there was no direct correlation between total insulin secretion during a 75 g oral glucose loading test and serum calcium or free fatty acid level. The findings that 1 alpha (OH)D3 enhances insulin secretion and reduces the levels of serum free fatty acid in non-insulin-dependent diabetics provide us with the possibility that vitamin D may play some role in the regulation of insulin secretion.

Adult↗
PubMed1985

12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulates somatostatin release from isolated perfused rat stomach.

Effect of TPA (12-O-tetradecanoyl phorbol-13-acetate), a potent tumor promoter, on immunoreactive somatostatin release was investigated using the isolated perfused rat stomach. TPA at the concentration as low as 20nM significantly stimulated the somatostatin release from isolated perfused rat stomach. The integrated net output of somatostatin induced by TPA was dose-dependent in a range of 5 - 50nM TPA. Since TPA is known to activate C-kinase specifically at a low dose (less than 20nM), these findings suggest that C-kinase system may be involved in the regulation of somatostatin release in rat stomach.

Animals↗
PubMed1985

Phorbol ester stimulates calcitonin secretion synergistically with A23187, and additively with dibutyryl cyclic AMP in a rat C-cell line.

The mechanism of action of 12-O-tetradecanoyl phorbol-13-acetate (TPA) on calcitonin secretion was studied in a rat C-cell line, rMTC 6-23. TPA stimulated calcitonin secretion at the concentration of 16nM. This effect was synergistically enhanced with calcium ionophore, A23187. Synthetic diacylglycerol, 1-oleoyl-2-acetyl-glycerol (OAG), also showed a synergism with A23187 on calcitonin secretion. When dibutyryl cyclic AMP was added with TPA, an additive effect was obtained. These data suggest that C-kinase might be a possible regulator of calcitonin secretion in addition to the cyclic AMP-mediated pathway.

Animals↗
PubMed1985

Improvement of chemical analysis of antibiotics. VIII. Application of prepacked C18 cartridge for the analysis of tetracycline residues in animal liver.

A simple, rapid and precise analytical method for tetracycline (TC) residues in the liver of slaughtered animals has been established. The recoveries of oxytetracycline (OTC), TC, chlortetracycline (CTC) and doxycycline (DC) from beef liver spiked at the level of 1.0 ppm were 87.7, 87.5, 79.6 and 67.5% with coefficients of variations of 1.01-2.87%. Detection limits in beef liver were 0.05 and 0.1 ppm for OTC and TC and for CTC and DC, respectively. It is also possible to apply this method to the analysis of residual TCs in various foods with the same recovery, accuracy and detection limits as in the case of beef liver.

Animals↗
PubMed1985

Time course study of insulin secretion after 1,25-dihydroxyvitamin D3 administration.

Vitamin D3 is known to be involved in pancreatic endocrine function. The rapidity of action of the biologically active form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], was studied over time (from 0-72 h) on pancreatic insulin secretion by the subsequently isolated perfused pancreas of vitamin D-deficient rats pair-fed with vitamin D-deficient control rats treated with vehicle alone. At 8 h after 1,25(OH)2D3 administration (1.3 nmol), augmentation of the insulin secretion in response to 16.6 mM glucose had already significantly appeared and reached a maximum at 14 h, and then markedly decreased to pretreatment baseline values by 36 h. In a separate experiment using 20 mM arginine as a stimulus, insulin secretion from the isolated perfused pancreas also showed a significant increase at 8 h and demonstrated a maximum response at 14 h after 1,25(OH)2D3 administration, followed by gradual decrease to 72 h. The prevailing levels of serum parameters, including calcium, phosphorus, and glucose, seemed not to be involved in this mechanism, since these were not correlated to the amount of insulin secretion by the subsequently isolated perfused pancreas. Also the observed rapid effects of 1,25(OH)2D3 on insulin secretion appear not to be related to a rapid effect of the secosteroid on increased dietary/caloric intake. These results clearly establish both the dependence of and rapid dynamics response of the perfused pancreas to the potentiating effects of in vivo administered 1,25(OH)2D3 on either glucose- or arginine-mediated insulin secretion from the perfused pancreas.

Animals↗
PubMed1985

Demonstration that the vitamin D metabolite 1,25(OH)2-vitamin D3 and not 24R,25(OH)2-vitamin D3 is essential for normal insulin secretion in the perfused rat pancreas.

It has previously been shown that vitamin D deficiency impairs arginine-induced insulin secretion from the isolated, perfused rat pancreas (Science 1980; 209:823-25). Since vitamin D is known to be metabolized to 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) and 24R,25-dihydroxyvitamin D3 (24,25[OH]2D3), it is essential to clarify which vitamin D metabolite has the important role of enhancing insulin secretion. In this report, a comparison is made of the relative efficacy of 3-wk repletion with vitamin D3 (980 pmol/day), 1,25(OH)2D3 (39 pmol/day or 195 pmol/day), and 24,25(OH)2D3 (650 pmol/day) on arginine-induced insulin secretion from the isolated, perfused rat pancreas; in this experiment, the daily caloric intake of the animals receiving vitamin D or its metabolites was controlled by pair feeding to the caloric intake of the vitamin D-deficient rats. 1,25(OH)2D3 repletion was found to completely restore insulin secretion to the levels seen in vitamin D3-replete, pair-fed controls in both the first and second phases, while 24R,25(OH)2D3 only partially improved insulin secretion, and then only in the first phase. Changes of both serum calcium levels and dietary caloric intake after vitamin D metabolite administration are concluded to play a lesser role on the enhancement of insulin secretion, since, in a separate experiment, vitamin D-deficient rats with normal serum calcium levels did not show recovery of insulin secretion equivalent to the vitamin D-replete animals under conditions of dietary pair feeding. These results suggest that 1,25(OH)2D3 but not 24,25(OH)2D3 plays an essential role in the normal insulin secretion irrespective of the dietary caloric intake and prevailing serum calcium levels.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Pancreatic vitamin D-dependent calcium binding protein: biochemical properties and response to vitamin D.

The biochemical properties of a chick pancreatic calcium binding protein (CaBP) and its response to vitamin D status and dietary calcium and phosphorus levels were studied and compared with the known vitamin D-dependent CaBPs present in the chick intestine and kidney. Pancreatic CaBP is homologous to the intestinal CaBP on the basis of immunological cross-reactivity, molecular size (28,200 Da), and charge properties (chromatographic mobility on DEAE-Sephadex in the presence of either EDTA or Ca2+). Pancreatic levels of CaBP respond to changes in vitamin D status and dietary Ca and P level in a fashion similar to the intestinal CaBP. Thus, in the absence of dietary vitamin D, both pancreatic and intestinal CaBPs were essentially undetectable, while in the presence of dietary vitamin D, a low dietary P (0.05%) elevated the pancreatic and intestinal CaBP 1.5X and 1.6X, respectively, compared to the CaBP levels present with normal dietary Ca and P (1.0%, 1.0%). The tissue levels of pancreatic CaBP (6-10 ng/mg protein) are about 0.2% of the intestine (5000 ng/mg protein) and 1% of the kidney CaBP (700 ng/mg protein). However, when corrections are made for the CaBP distribution in the tissues and expressed as CaBP concentration per CaBP-containing cells, the pancreatic CaBP level was 30% of the intestine and 10% of the kidney. Collectively, these results suggest that the chick pancreatic vitamin D-dependent CaBP is a homologous protein to the intestinal CaBP, both with regards to its relative cellular concentration as well as in its response to changing dietary levels of Ca and P.

Animals↗
PubMed1984

Dietary vitamin D is essential for normal insulin secretion from the perfused rat pancreas.

We have reported previously that arginine-induced insulin secretion was impaired in the vitamin D-deficient rat pancreas, and that it was improved by dietary vitamin D repletion (Norman, A. W., B. J. Frankel, A. M. Heldt, and G. M. Grodsky, 1980, Science [Wash. DC]. 209:823-825). In this study, we evaluate in the perfused rat pancreas system whether the effects of vitamin D and its metabolites on insulin secretion are direct in action on the pancreas and limited to the secretagogue arginine, or whether they are secondary to the hypocalcemia or reduced caloric and calcium intake associated with vitamin D deficiency. In an experiment where vitamin D-replete (+D) rats were pair-fed to D-deficient (-D) rats fed ad lib., the secretion of insulin in response to arginine infusion in the +D perfused rat pancreas was threefold higher than in the -D control. In a second experiment, the serum calcium level was elevated from the characteristic hypocalcemic level of -D rats (4.9 +/- 0.1 mg/dl) to a normal calcemic level (10.0 +/- 0.3 mg/dl) by feeding the rats a -D diet with dietary calcium levels ranging from 0.4 to 4%. In these -D rats, the pancreatic perfusion study with the secretagogue arginine showed a similar blunted insulin secretion response in all groups in spite of the significant differences of serum calcium levels. In a third experiment, insulin secretion in response to the separate administration of arginine (10 mM), glucose (16.9 mM), and tolbutamide (0.37 mM) was found to be significantly higher in pair-fed, normocalcemic +D rats than in -D rats with normal calcium levels. These results indicate that vitamin D or its metabolites are essential for normal insulin secretion and that the dietary intake of calcium and the resulting serum calcium levels play a lesser role than vitamin D availability in mediating insulin secretion.

Animals↗
PubMed1984

Bullous amyloidosis associated with Bence Jones proteinemia without proteinuria.

A 74 yo female was found to have bullous dermal amyloidosis on the background of systemic amyloidosis with multiple myeloma. There was monoclonal immunoglobulin light chain of kappa type in the serum with no proteinuria (Bence Jones proteinemia without Bence Jones proteinuria), along with proliferations of kappa-producing plasma cells in the marrow.

Aged↗
PubMed1983

Effect of tolbutamide on insulin, glucagon, and somatostatin release from the diabetic rat pancreas with special reference to glucose concentration.

The effects of tolbutamide on insulin, glucagon, and somatostatin secretion were investigated in the isolated perfused pancreas from normal and diabetic rats under low (30 mg/dl), normal (100 mg/dl), and high (300 mg/dl) glucose conditions. In the normal rat pancreas, tolbutamide-induced insulin release was increased when the glucose concentration in the perfusion medium was increased from 30-300 mg/dl. Tolbutamide had an inhibitory effect on glucagon release at the low (30 mg/dl) glucose concentrations, although a stimulatory effect was observed under normoglycemic conditions. The total amount of somatostatin secretion above baseline during tolbutamide infusion was higher under the normal glucose than under the low glucose condition. However, further augmentation of somatostatin release was not found at the high glucose concentration. In the diabetic rat pancreas, insulin release was diminished and tolbutamide-induced somatostatin release was enhanced with increasing glucose concentrations. Glucagon release was stimulated at the normal glucose concentration, but inhibited temporarily at the high glucose concentration. The maximum somatostatin response in the early phase was significantly decreased in the diabetic pancreas under low and normal glycemic conditions, when expressed as an incremental change (percentage) above baseline. From these results, one can conclude: (1) tolbutamide has a stimulatory effect on the pancreatic D cell in both the normal and diabetic pancreas; (2) the early response of somatostatin is decreased in the diabetic pancreas, except under conditions of high glucose concentration; and (3) the pancreatic A cell response to tolbutamide was not uniform and was quite different from the response of the D cell.

Animals↗
PubMed1983

[Effect of suloctidil in the protection of the cerebral function].

It has been demonstrated that suloctidil [erythro-1-(4-isopropylthiophenyl)-2-n-octylaminopropanol] has a protective effect against cerebral hypoxia to elongate the survival time of mice subjected to normobaric hypoxia (96% N2 + 4% O2 gas mixture). In this study, further experiments were done to elucidate the mechanism of protection against cerebral hypoxia with a variety of experimental models. Pretreatment (30 min) with suloctidil (12.5-50 mg/kg, i.p.) increased the number of gasping in the decapitated head of mouse as a complete ischemic model. Pyrithioxine (25, 50 mg/kg, i.p.) or cinnarizine (50, 100 mg/kg, i.p.) did not increase the gasping number. In the histotoxic anoxia with KCN (4 mg/kg, i.v.) in mice, suloctidil showed 30.8% and 46.2% survival rates at the doses of 25 and 50 mg/kg, i.p., respectively. Concerning this result, it has been revealed that suloctidil did not have any methemoglobin formation liability in rats (unpublished). Pyrithioxine did not show such protection following the injection of 12.5-50 mg/kg, i.p.. Suloctidil (3.0-50 mg/kg, i.p.) and pyrithioxine (3.0, 10 mg/kg, i.p.) significantly prolonged the survival time of mice subjected to hypobaric hypoxia (210 mmHg). In this cerebral hypoxia model, suloctidil kept glucose at a significantly higher level and lactate at a lower level in the brain of mice that were administered this drug than the control group. ATP was kept at higher level after suloctidil than the control under hypobaric hypoxia. Taking these evidences together, it can be concluded that suloctidil exerts its cerebral anti-hypoxic effect through cerebral glucose metabolism coupled with oxidative phosphorylation to yield the high energy substance ATP in a variety of models tested in this study. The fact obtained in this study, together with increase in cerebral blood flow by suloctidil, may also elucidate the protective effect of suloctidil against cerebral hypoxia.

Animals↗