Exenatide Activates the APPL1-AMPK-PPARα Axis to Prevent Diabetic Cardiomyocyte ApoptosisReportar como inadecuado

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Journal of Diabetes ResearchVolume 2016 2016, Article ID 4219735, 10 pages

Research ArticleEndocrine Department, The First Affiliated Hospital of the Third Military Medical University, Chongqing 400038, China

Received 31 March 2015; Revised 7 June 2015; Accepted 10 June 2015

Academic Editor: Nicoleta Alexandru

Copyright © 2016 Lei XiaoTian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To investigate the effect and mechanism of the exenatide on diabetic cardiomyopathy. Methods. Rats were divided into control group, diabetes group D, diabetes treated with insulin DI group, and diabetes treat with exenatide DE group. We detected apoptosis rate by TUNEL, the adiponectin and high molecular weight adiponectin HMW-adiponectin by ELISA, and the expression of APPL1, p-AMPK-T-AMPK, PPARα, and NF-κB by immunohistochemistry and western blotting. Results. Compared with the D group, the apoptosis in the Control and DE groups was decreased ; the adiponectin and HMW-adiponectin were increased ; the APPL1, p-AMPK-T-AMPK, PPARα, and LV −dP-dt were increased ; and the NF-κB, GRP78, and LVEDP were decreased . Compared with DE group, the glucose levels in the DI group were similar ; the apoptosis and LVEDP were increased; the APPL1, p-AMPK-T-AMPK, PPARα, and LV −dP-dt were decreased ; the NF-κB and GRP78 were increased ; the adiponectin and HMW-adiponectin were significantly decreased . Conclusion. Our model of diabetic cardiomyopathy was constructed successfully. After being treated with exenatide, the adiponectin and HMW-adiponectin and the APPL1-AMPK-PPARα axis were increased, the NF-κB and the apoptosis were decreased, the cardiac function of the diabetic rats was improved, and these effects were independent of glucose control.

Autor: Lei XiaoTian, Wu QiNan, Gan XiaGuang, Deng WuQuan, Chen Bing, and Liang ZiWen

Fuente: https://www.hindawi.com/


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