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Experimental & Molecular Medicine ; : 12-17, 2000.
Article in English | WPRIM | ID: wpr-16701

ABSTRACT

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.


Subject(s)
Adenosine Triphosphate/pharmacology , Adenosine Triphosphate/metabolism , Alloxan/pharmacology , Animals , B-Lymphocytes/metabolism , B-Lymphocytes/drug effects , B-Lymphocytes/cytology , Calcium/pharmacology , Cell Line , Cell Nucleus/genetics , Cell Nucleus/drug effects , Cell Survival , DNA/metabolism , DNA/genetics , DNA/drug effects , DNA Fragmentation , Dose-Response Relationship, Drug , Egtazic Acid/pharmacology , Glucose/pharmacology , Insulin/metabolism , Oligomycins/pharmacology
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