Document Detail


Reactive oxygen species and insulin-resistant cardiomyopathy.
MedLine Citation:
PMID:  19671065     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. The prevalence of insulin resistance has increased markedly in the past decade and is known to be associated with cardiovascular risk. Evidence of an insulin-resistant cardiomyopathy, independent of pressure or volume loading influences, is now emerging. 2. Cardiac oxidative stress is often observed coincident with insulin resistance and there is accumulating evidence that reactive oxygen species (ROS) mediate deleterious effects in the insulin-resistant heart. It is established that ROS modification of signalling proteins can adversely modulate cellular processes, leading to cardiac growth remodelling and dysfunction. The mechanisms of ROS-induced damage in insulin-resistant cardiomyopathy are yet to be fully elucidated. 3. A number of different animal models have been used to study cardiac insulin resistance, including high-sugar dietary interventions, genetically modified diabetic mice and streptozotocin-induced diabetes. Mechanistic studies manipulating cardiac anti-oxidant levels, either endogenously or exogenously, in these models have demonstrated a role for ROS in the cardiac manifestations associated with insulin resistance. 4. The present review summarizes the cardiac-specific characteristics of insulin resistance, the features of cardiac metabolism relevant to ROS generation and ROS-mediated cardiomyocyte damage pathways. In vivo studies in which a combination of genetic and environmental variables have been manipulated are considered. These studies provide particular insights into the induction and suppression of insulin-resistant cardiomyopathy.
Authors:
Kimberley M Mellor; Rebecca H Ritchie; Lea M D Delbridge
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2009-08-04
Journal Detail:
Title:  Clinical and experimental pharmacology & physiology     Volume:  37     ISSN:  1440-1681     ISO Abbreviation:  Clin. Exp. Pharmacol. Physiol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-24     Completed Date:  2010-06-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0425076     Medline TA:  Clin Exp Pharmacol Physiol     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  222-8     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies / etiology*,  metabolism
Diabetes Mellitus, Experimental / metabolism
Dietary Sucrose / administration & dosage
Energy Metabolism / physiology
Free Radical Scavengers / metabolism
Humans
Insulin Resistance*
Mice
Mitochondria, Heart / metabolism,  pathology
Myocardium / metabolism,  pathology
Oxidative Stress / physiology
Rats
Reactive Oxygen Species / metabolism*
Chemical
Reg. No./Substance:
0/Dietary Sucrose; 0/Free Radical Scavengers; 0/Reactive Oxygen Species

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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