High glucose stimulates glutamate uptakes in pancreatic beta-cells / 한국실험동물학회지
Laboratory Animal Research
; : 327-331, 2011.
Article
in En
| WPRIM
| ID: wpr-45069
Responsible library:
WPRO
ABSTRACT
Pancreatic beta-cells are major cells responsible for glucose metabolism in the body. Hyperglycemia is known to be a primary factor in the induction of diabetes mellitus. Glutamate is also an excitatory neurotransmitter in diverse organs. Oxidative stress also plays a pivotal role in the development of diabetes mellitus. However, the effect of hyperglycemia in glutamate uptake in the pancreas is not clear. Furthermore, the relationship between high glucose-induced glutamate uptake and oxidative stress has not been investigated. Therefore, this study was conducted to investigate the effect of high glucose on glutamate uptake in pancreatic beta-cells. In the present study, 25 mM glucose stimulated the glutamate uptake in HIT-15 cells of hamster pancreatic beta-cells. The treatment of 25 mM glucose and 1 mM glutamate also decreased the cell viability in HIT-15 cells. In addition, the treatment of 25 mM glucose induced an increase of lipid peroxide formation. High glucose-induced increase of LPO formation was prevented by the treatment of antioxidants such as N-acetyl-L-cysteine and quercetin. Furthermore, high glucose-induced stimulation of glutamate uptake and decrease of cell viability were also blocked by the treatment of N-acetyl-L-cysteine and quercetin. In conclusion, high glucose stimulated glutamate uptake via oxidative stress in pancreatic beta-cells.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Pancreas
/
Acetylcysteine
/
Quercetin
/
Cell Survival
/
Oxidative Stress
/
Neurotransmitter Agents
/
Glutamic Acid
/
Diabetes Mellitus
/
Glucose
/
Hyperglycemia
Limits:
Animals
Language:
En
Journal:
Laboratory Animal Research
Year:
2011
Type:
Article