Inhibition by Calcium Antagonist of Coupling of Insulin Binding and Insulin Action on Glucose Transport in Isolated Fat Cells

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Title ( eng )
Inhibition by Calcium Antagonist of Coupling of Insulin Binding and Insulin Action on Glucose Transport in Isolated Fat Cells
Title ( jpn )
単離脂肪細胞におけるカルシウム拮抗剤によるインスリン結合とブドウ糖輸送に対するインスリン作用の coupling に及ぼす阻害作用
Creator
Ishibashi Fukashi
Kubo Keiji
Source Title
Hiroshima Journal of Medical Sciences
Volume 33
Issue 1
Start Page 73
End Page 79
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
In the present study we examined the influence of calcium antagonist, nicardipine-HCl, on insulin binding and insulin action on glucose transport in isolated fat cells. The calcium antagonist did not influence the time course of 125I-insulin binding or the insulin concentration required for 50% displacement of 125I-insulin binding. Calcium antagonist prolonged the lag time of insulin action on glucose transport. Calcium antagonist, however, did not influence the insulin concentration required for half maximal response. The prolongation of the lag time was also seen with 2 different calcium antagonists (verapamil and diltiazem-HCl). Calcium antagonists might impair the transmission of signal from insulin receptor by other mechanism(s) rather than the inhibition of transmembrane transport of calcium, because calcium antagonist did not inhibit 45Ca uptake and efflux from preloaded fat cells, and because known calmodulin inhibitors (trifluoperazine and prochlorperazine) prolonged the lag time for insulin action without influence on insulin concentration for the half maximal response.

In conclusion calcium antagonist might act to calmodulin, phospholipids or membrane proteins.
Keywords
3-O-methylgucose uptake
Calmodulin inhibitors
45Ca flux
Log time of insulin action
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University School of Medicine
Date of Issued 1984-03
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312
[PMID] 6384143