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Experimental & Molecular Medicine ; : 12-17, 2000.
Artigo em Inglês | WPRIM | ID: wpr-16701

RESUMO

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.


Assuntos
Trifosfato de Adenosina/farmacologia , Trifosfato de Adenosina/metabolismo , Aloxano/farmacologia , Animais , Linfócitos B/metabolismo , Linfócitos B/efeitos dos fármacos , Linfócitos B/citologia , Cálcio/farmacologia , Linhagem Celular , Núcleo Celular/genética , Núcleo Celular/efeitos dos fármacos , Sobrevivência Celular , DNA/metabolismo , DNA/genética , DNA/efeitos dos fármacos , Fragmentação do DNA , Relação Dose-Resposta a Droga , Ácido Egtázico/farmacologia , Glucose/farmacologia , Insulina/metabolismo , Oligomicinas/farmacologia
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