Lab Anim Res.  2011 Dec;27(4):327-331. 10.5625/lar.2011.27.4.327.

High glucose stimulates glutamate uptakes in pancreatic beta-cells

Affiliations
  • 1Department of Veterinary Physiology, College of Veterinary Medicine, Seoul National University, Seoul, Korea.
  • 2Bio-therapy Human Resources Center, Animal Medical Center, Department of Veterinary Physiology, College of Veterinary Medicine, Chonnam National University, Gwangju, Korea. parksh@chonnam.ac.kr

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.

Keyword

Pancreatic beta-cells; hyperglycemia; glutamate uptake; oxidative stress
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