Glucagon-like peptide 1 improves learning and memory abilities of rats with type 2 diabetes.
- Author:
Zhao-Guang TAN
1
,
2
,
3
;
Wei-Hong GAO
;
Xiang-Sheng CAI
;
Fang WANG
;
Hong-Xiang HUI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Diabetes Mellitus, Experimental; drug therapy; Diabetes Mellitus, Type 2; drug therapy; Glucagon-Like Peptide 1; pharmacology; Hippocampus; drug effects; Learning; drug effects; Male; Memory; drug effects; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; Streptozocin
- From: Journal of Southern Medical University 2016;36(10):1345-1351
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of glucagon-like peptide 1 (GLP-1) on cognitive dysfunction in diabetic rats.
METHODSMale SD rats were randomly divided into normal control group, diabetes mellitus (DM) group, and GLP-1 treatment group. Rat models of type 2 diabetes were established by high-sugar and high-fat feeding and streptozotocin (STZ) injection, and 25 days after the onset of diabetes, GLP-1 was infused in GLP-1 treatment group at the rate of 30 pmol·kg·minvia a subcutaneous osmotic pump for 7 days. The learning and cognitive ability of the rats was assessed with Morris water maze test, and the expression of cognition-related genes in the hippocampus tissue was detected with real-time PCR, Western blotting and immunohistochemical staining.
RESULTSCompared with the normal control group, the diabetic rats showed significantly decreased learning and memory abilities (P<0.05) with increased hippocampal expressions of APP, BACE1, Arc, ERK1/2, PKA, and PKC mRNAs (P<0.05) and Arc protein. Compared with diabetic rats, GLP-1-treated rats showed significantly improvements in the learning and memory function (P<0.05) with decreased expressions of APP, BACE1, Arc, ERK1/2, and PKA mRNAs (P<0.05) and Arc protein.
CONCLUSIONGLP-1 can improve cognitive dysfunctions in diabetic rats possibly by regulating the PKC, PKA, and ERK1/2 pathways and inhibiting Arc expression in the hippocampus.