J Korean Diabetes Assoc.  1999 Aug;23(4):530-540.

Protective Mechanism of Glucose against Alloxan-Indeved HIT-T15 Cell Damage

• Lee TH
• Park TS
• Kim HR

Abstract

BACKGROUND: Glucose prevents the development of alloxan-induced diabetes, but the precise protective mechanism of glucose is not yet clearly known.
METHODS
The protective mechanism of glucose on alloxan-induced B-cell damage as investigated using a Syrian hamster transformed B-cell line,HIT-T15 cells.
RESULTS
Alloxan caused cell death, inhibition of insulin release, elevation of cytosolic free Ca, DNA fragmentation and decrease of cellular NAD+and ATP. However, pretreatment of HIT-T15 ce]ls with glucose significantly blocked DNA fragmentation, depletion of intracellular NAD+,ATP and cell viability induced by alloxan, but did not affect the increase of cytosolic free Ca2+.The result indicate that glucose acts between Ca2+ influx and DNA fragmentation on a chain of reactions in the diabetogenesis of alloxan.
CONCLUSION
These protective effects of glucose on alloxan-induced B-cell damage werepletely abolished by pretreatment with inhibitors of glucose-6-phosphate dehydrogenase, dehydroepian- drosterone (DHEA) and epiandrosterone (EPI), suggesting that a metabolic intermediate, such as NADPH, produced from glucose through pentose phosphate pathway plays an important role in the protection of B-cell damage by alloxan.

Keyword

Key Words; Alloxan; glucose; B-cell

MeSH Terms

Adenosine Triphosphate
Alloxan
Androsterone
Animals
B-Lymphocytes
Cell Death
Cell Survival
Cricetinae
Cytosol
DNA Fragmentation
Glucose*
Glucosephosphate Dehydrogenase
Insulin
NADP
Pentose Phosphate Pathway
Adenosine Triphosphate
Alloxan
Androsterone
Glucose
Glucosephosphate Dehydrogenase
Insulin
NADP