High glucose stimulates glutamate uptakes in pancreatic β-cells

Abstract

Pancreatic β-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 β-cells. In the present study, 25 mM glucose stimulated the glutamate uptake in HIT-15 cells of hamster pancreatic β-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 β-cells.

Defining the Human Adipose Tissue Proteome To Reveal Metabolic Alterations in Obesity

“…Glutamate also has a major role in the function of neural and non-neural tissues . Moreover, evidence for the association of the high glucose-induced stimulation of glutamate with the apoptosis of pancreatic β-cells has been provided . Thus, suppression of BCAT1 may contribute to a lower production of glutamate and reduced consumption of AKG, resulting in increased levels of AKG that can thereby enter the TCA cycle.…”