[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.


CONCLUSIONS
Overproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process.
Qu
Zhong-sen
ZS
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Tian
Qing
Q
Zhou
Xin-Wen
XW
Wang
Xiao-chuan
XC
Wang
Qun
Q
Zhang
Qi
Q
Wang
Jian-zhi
JZ
D000544:Alzheimer Disease / Q000209:etiology*; D027322:Amino Acid Transport System X-AG / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D018021:Lithium Chloride / Q000494:pharmacology; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D027322:Amino Acid Transport System X-AG; D016229:Amyloid beta-Peptides; D038362:Glycogen Synthase Kinase 3; D018021:Lithium Chloride