short-chain fatty acid propionate alleviates akt2 knockout-induced myocardial contractile dysfunction短链脂肪酸丙酸减轻akt2 knockout-induced心肌收缩功能障碍.pdfVIP

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short-chain fatty acid propionate alleviates akt2 knockout-induced myocardial contractile dysfunction短链脂肪酸丙酸减轻akt2 knockout-induced心肌收缩功能障碍.pdf

short-chain fatty acid propionate alleviates akt2 knockout-induced myocardial contractile dysfunction短链脂肪酸丙酸减轻akt2 knockout-induced心肌收缩功能障碍

Hindawi Publishing Corporation Experimental Diabetes Research Volume 2012, Article ID 851717, 10 pages doi:10.1155/2012/851717 Research Article Short-Chain Fatty Acid Propionate Alleviates Akt2 Knockout-Induced Myocardial Contractile Dysfunction Linlin Li,1, 2 Yinan Hua,2 and Jun Ren2 1 Department of Pharmacology, Xinjiang Medical University, Xinjiang, Urumqi 830011, China 2 Center for Cardiovascular Research and Alternative Medicine, College of Health Sciences, University of Wyoming, Laramie, WY 82071, USA Correspondence should be addressed to Jun Ren, jren@uwyo.edu Received 27 June 2011; Accepted 1 August 2011 Academic Editor: Yingmei Zhang Copyright © 2012 Linlin Li 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. Background and Aims. Dysregulation of Akt has been implicated in diseases such as cancer and diabetes, although little is known about the role of Akt deficiency on cardiomyocyte contractile function. This study was designed to examine the effect of Akt2 knockout-induced cardiomyocyte contractile response and the effect of dietary supplementation of short-chain fatty acid propionate on Akt2 knockout-induced cardiac dysfunction, if any. Methods and Results. Adult male wild-type (WT) and Akt2 knockout mice were treated with propionate (0.3 g/kg, p.o.) or vehicle for 7 days. Oral glucose tolerance test (OGTT) was performed. Cardiomyocyte contractile function and mitochondrial membrane potential were assessed. Expression of insulin- signaling molecules Akt, PTEN, GSK3β, and eNOS receptors for short-chain fatty acids GPR41, and GPR43 as well as protein phosphat

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