[Alteration of beta-amyloid and glutamate transporter in the brain of diabetes rats and the underlying mechanism].

OBJECTIVE: To investigate the alteration of beta-amyloid (Abeta) and glutamate transporter in the brain cortex of diabetes mellitus (DM) rats and the underlying mechanism.
METHODS: The rats were randomly divided into control, DM, DM +NaCl, and DM +LiCl groups and diabetes was induced by streptozotocin. The activity of glycogen synthase kinase-3 (GSK-3) and the function of glutamate transporter were measured by 32P-labelling. The amount of Abeta was determined by enzyme-linked immunosorbentassay.
RESULTS: In DM group, the level of Abeta40 increased (P < 0.01), but the function of glutamate transporter was impaired (P < 0.05). The activity of GSK-3 was stimulated (P < 0.05). Compared with DM group, the level of Abeta40 was restored (P < 0.01), and the function of glutamate transporter was enhanced (P < 0.05) in LiCl treated group, accompanied by a decreased activity of GSK-3.
CONCLUSION: Overproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process.