Protective mechanism of glucose against alloxan-induced beta-cell damage: pivotal role of ATP.
- Author:
Hye Won RHO
1
;
Ji Na LEE
;
Hyung Rho KIM
;
Byung Hyun PARK
;
Jin Woo PARK
Author Information
1. Department of Biochemistry, School of Medicine and Institute for Medical Science, Chonbuk National University, Chonju, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
glucose;
ATP;
alloxan;
diabetes;
DNA fragmentation
- MeSH:
Adenosine Triphosphate/pharmacology;
Adenosine Triphosphate/metabolism;
Alloxan/pharmacology*;
Animal;
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/secretion;
Oligomycins/pharmacology
- From:Experimental & Molecular Medicine
2000;32(1):12-17
- CountryRepublic of Korea
- Language:English
-
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.
