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Article de Anglais | WPRIM | ID: wpr-16701

RÉSUMÉ

Glucose prevents the development of diabetes induced by alloxan. In the present study, the protective mechanism of glucose against alloxan-induced beta-cell damage was investigated using HIT-T 15 cell, a Syrian hamster transformed beta-cell line. Alloxan caused beta-cell damages with DNA fragmentation, inhibition of glucose-stimulated insulin release, and decrease of cellular ATP level, but all of these beta-cell damages by alloxan were prevented by the presence of 20 mM glucose. Oligomycin, a specific inhibitor of ATP synthase, completely abolished the protective effects of glucose against alloxan-induced cell damage. Furthermore, treatment of nuclei isolated from HIT-T15 cells with ATP significantly prevented the DNA fragmentation induced by Ca2+. The results indicate that ATP produced during glucose metabolism plays a pivotal role in the protection of glucose against alloxan-induced beta-cell damage.


Sujet(s)
Adénosine triphosphate/pharmacologie , Adénosine triphosphate/métabolisme , Alloxane/pharmacologie , Animaux , Lymphocytes B/métabolisme , Lymphocytes B/effets des médicaments et des substances chimiques , Lymphocytes B/cytologie , Calcium/pharmacologie , Lignée cellulaire , Noyau de la cellule/génétique , Noyau de la cellule/effets des médicaments et des substances chimiques , Survie cellulaire , ADN/métabolisme , ADN/génétique , ADN/effets des médicaments et des substances chimiques , Fragmentation de l'ADN , Relation dose-effet des médicaments , Acide egtazique/pharmacologie , Glucose/pharmacologie , Insuline/métabolisme , Oligomycines/pharmacologie
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