Alteration of beta-amyloid and glutamate transporter in the brain of diabetes rats and the underlying mechanism.
- Author:
Zhong-sen QU
1
;
Qing TIAN
;
Xin-Wen ZHOU
;
Xiao-chuan WANG
;
Qun WANG
;
Qi ZHANG
;
Jian-zhi WANG
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; etiology; Amino Acid Transport System X-AG; metabolism; Amyloid beta-Peptides; metabolism; Animals; Cerebral Cortex; metabolism; Diabetes Mellitus, Experimental; complications; drug therapy; physiopathology; Glycogen Synthase Kinase 3; metabolism; Lithium Chloride; pharmacology; Male; Random Allocation; Rats; Rats, Sprague-Dawley
- From: Acta Academiae Medicinae Sinicae 2005;27(6):708-711
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the alteration of beta-amyloid (Abeta) and glutamate transporter in the brain cortex of diabetes mellitus (DM) rats and the underlying mechanism.
METHODSThe 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.
RESULTSIn 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.
CONCLUSIONOverproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process.
