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. 2013:2013:689841.
doi: 10.1155/2013/689841. Epub 2013 Jun 17.

Effects of amyloid precursor protein 17 peptide on the protection of diabetic encephalopathy and improvement of glycol metabolism in the diabetic rat

Heng Meng  1 , Duo Zhang, Haishan Yang
Affiliations

Effects of amyloid precursor protein 17 peptide on the protection of diabetic encephalopathy and improvement of glycol metabolism in the diabetic rat

Heng Meng et al. J Diabetes Res. 2013.

Abstract

Researchers have proposed that amyloid precursor protein 17 peptide (APP17 peptide), an active fragment of amyloid precursor protein (APP) in the nervous system, has therapeutic effects on neurodegeneration. Diabetic encephalopathy (DE) is a neurological disease caused by diabetes. Here we use multiple experimental approaches to investigate the effect of APP17 peptide on changes in learning behavior and glycol metabolism in rats. It was found that rats with DE treated by APP17 peptide showed reversed behavioral alternation. The [(18)F]-FDG-PET images and other results all showed that the APP17 peptide could promote glucose metabolism in the brain of the DE rat model. Meanwhile, the insulin signaling was markedly increased as shown by increased phosphorylation of Akt and enhanced GLUT4 activation. Compared with the DE group, the activities of SOD, GSH-Px, and CAT in the rat hippocampal gyrus were increased, while MDA decreased markedly in the DE + APP17 peptide group. No amyloid plaques in the cortex and the hippocampus were detected in either group, indicating that the experimental animals in the current study were not suffering from Alzheimer's disease. These results indicate that APP17 peptide could be used to treat DE effectively.

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Figures

Figure 1
Figure 1
(a) Blood glucose and (b) body weight of mice in 3 groups. (c) The ability analysis of learning and memory of mice in 3 groups.
Figure 2
Figure 2
Evaluation of brain glycometabolism in DE animals by PET/CT.
Figure 3
Figure 3
Enhanced insulin-induced Akt activation in the hippocampal gyrus of DE rats with APP17 treatment.
Figure 4
Figure 4
Enhanced GLUT4 expression in the hippocampal gyrus of DE rats with APP17 treatment.
Figure 5
Figure 5
Enhanced insulin-induced glucose transport in PC-12 cells treated with APP17 peptide via PI3K-Akt pathway. Akt and PI3K inhibited cells pretreated with Akt inhibitor 124005; Akt non- PI3K inhibited cells were pretreated with Akt inhibitor 124011.
See this image and copyright information in PMC

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