Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/9469
Title: Protective effects of Desacyl Ghrelin on diabetic cardiomyopathy
Authors: Pei, XM
Yung, BY 
Yip, SP 
Chan, LW
Wong, CS 
Ying, M 
Siu, PM 
Keywords: Autophagy
Cardiomyopathy
Fibrosis
Ghrelin
Type 2 diabetes mellitus
Issue Date: 2015
Publisher: Springer
Source: Acta diabetologica, 2015, v. 52, no. 2, p. 293-306 How to cite?
Journal: Acta diabetologica 
Abstract: Aim: Diabetic cardiomyopathy is a specific complication of type 2 diabetes mellitus, which causes progressive cardiac dysfunction. Desacyl ghrelin has been preliminarily demonstrated to have beneficial effects on cardiovascular system and glucose metabolism, which are both related to diabetic cardiomyopathy. The aim of this study was to investigate the protective effects of desacyl ghrelin on cardiac dysfunction, cardiac fibrosis, and cellular autophagy in a type 2 diabetic mouse model. Materials and methods: Fourteen- to eighteen-week-old db/db diabetic and db/+ non-diabetic mice were intraperitoneally treated with desacyl ghrelin at a dosage of 100?£gg/kg for ten consecutive days. Ventricular fractional shortening was examined as an indicator of cardiac function by transthoracic echocardiography. Results: The presence of diabetic cardiomyopathy was evident by the reduction in fractional shortening shown in our examined db/db mice. Intriguingly, this reduction in fractional shortening was not observed in the hearts of db/db mice treated with desacyl ghrelin. Cardiac fibrosis (indicated by excessive collagen deposition, decreased by Adiponectin and Mmp13 expression, and up-regulated by Mmp8 expression) and impairment of autophagic signalling (indicated by decreases in Foxo3 and LC3 II-to-LC3 I ratio) were shown in the hearts of diabetic mice. All these cellular and molecular alterations were alleviated by desacyl ghrelin treatment. The key cardiac pro-survival cellular signals including AMPK, Akt, ERK1/2, and GSK3£\/£] were impaired in the diabetic hearts, but the adm
URI: http://hdl.handle.net/10397/9469
ISSN: 0940-5429
EISSN: 1432-5233
DOI: 10.1007/s00592-014-0637-4
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