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Biomedical subjects

T Toyota

Publications and source records attributed to T Toyota.

At least 415 records · Page 23Linked to original sources

Inhibitory action of rat insulin and synthetic rat C-peptide on insulin secretion in the perfused rat pancreas.

In order to determine whether both insulin and C-peptide have an inhibitory action on insulin secretion, the isolated rat pancreas was perfused with exogenous rat insulin or synthetic rat C-peptide in the presence of high or low concentration of glucose. In the presence of 2.8 mM glucose, exogenous rat insulin (4 or 10 ng/ml) and C-peptide 1 and 2 (100 ng/ml) show no effect on the insulin levels in the outflow from the perfused pancreas. However, the insulin response to 16.7 mM glucose decreased in the presence of exogenous rat insulin or synthetic rat C-peptide, showing a biphasic pattern of glucose-induced insulin release. When rat insulin or C-peptide were added at 20 min and removed at 40 min while the isolated pancreas was exposed to a 60-min glucose infusion (16.7 mM), glucose-induced insulin secretion decreased during the infusion of rat insulin or C-peptide. The present study clearly showed that exogenous rat insulin and synthetic rat C-peptide 1 and 2 inhibited glucose-induced insulin secretion. Although the suppressive mechanisms of the exogenous insulin and the C-peptide on insulin release are not yet proved, the inhibitory process is considered to be related to cyclic AMP in the pancreatic B-cell.

Animals↗

Influence of oral adsorbent AST-120 on anticonvulsive effect of zonisamide in rats.

The influence of oral adsorbent AST-120 (Kremezin) on the anticonvulsive effect and pharmacokinetics of zonisamide was investigated. Oral administration of zonisamide (50 mg/kg) blocked the appearance of the tonic extension induced by maximal electroshock seizure. This effect of zonisamide was inhibited by the oral coadministration of AST-120 (5 g/kg). In pharmacokinetics study, the serum zonisamide concentration after coadministration of zonisamide and AST-120 was significantly lower than that of single administration of zonisamide. However, the anticonvulsive effect of zonisamide was not affected by the administration of AST-120 1.5 h after zonisamide administration. In this condition, the serum zonisamide concentration was not changed. In the in vitro study, AST-120 completely adsorbed zonisamide. These findings suggest that when AST-120 is administered concurrently with zonisamide, a significant inhibition of the anticonvulsive effect of zonisamide occurs, and the decrease in serum zonisamide concentration by the adsorption effect of AST-120 is related to this phenomenon.

Administration, Oral↗

Antitumor agents, 104. Isolation of yadanziosides M and P from Brucea antidysenterica and identification of bruceantinoside B as a mixture of yadanzioside P and bruceantinoside C.

Yadanziosides M [3] and P [1] were isolated from Brucea antidysenterica. Their structures were elucidated by spectral data. Bruceantinoside B reported previously was reinvestigated and revealed to be a mixture of yadanzioside P and bruceantinoside C [2]. The structure of yadanzioside P was found to be identical to that of bruceantinoside B.

Antineoplastic Agents, Phytogenic↗

Antitumor agents, 118. The isolation and characterization of bruceanic acid A, its methyl ester, and the new bruceanic acids B, C, and D, from Brucea antidysenterica.

The known bruceanic acid A [1] and its methyl ester 2, as well as the new bruceanic acids B [3], C [4], and D [5], have been isolated from Brucea antidysenterica. The structures of 1-5 were elucidated by spectral data. Compound 1 demonstrated cytotoxicity against KB and TE671 tumor cells. Compound 5 was cytotoxic against P-388 lymphocytic leukemia cells.

Animals↗

The prevalence of mitochondrial gene mutations in childhood diabetes in Japan.

To investigate the prevalence of mitochondrial DNA mutations among Japanese children with IDDM as well as in those with NIDDM, a total of 155 patients with IDDM and 30 patients with NIDDM who were younger than 15 years of age at onset were studied for the following mtDNA mutations: 1) the A-->G mutation at position 3243 of mitochondrial leucine transfer RNA (3243 mutation); 2) the G-->A mutation at position 3316 of mitochondrial leucine transfer RNA (3316 mutation), and 3) The T-->C mutation at position 3394 of the mitochondrial NADH dehydrogenase subunit (3394 mutation). None of the 155 IDDM patients had the 3243 mutation. Although two of the 155 IDDM patients had homoplasmy of 3316 and five had 3394 mutations, these frequencies were not significant compared with healthy controls. None of the 30 NIDDM patients had the 3243, 3316 or 3394 mutation. The presence of these mutations even in control subjects suggests that the effect of the 3316 or 3394 mutation on mitochondrial function is relatively mild. It seems that 3316 and 3394 mutations contribute to the manifestation of diabetes together with other genetic and/or environmental factors.

Adolescent↗