Document Detail

Myocardial susceptibility to ischemic-reperfusion injury in a prediabetic model of dietary-induced obesity.
MedLine Citation:
PMID:  18359896     Owner:  NLM     Status:  MEDLINE    
We assessed the myocardial susceptibility to ischemic-reperfusion injury in obese rat hearts in the absence and the presence of predicted circulating concentrations of insulin and fatty acids. Feeding rats a high-calorie diet resulted in increases in body weight, visceral fat content, cardiac hypertrophy, plasma insulin, nonesterified free fatty acid, and triglyceride concentrations. In the absence of both insulin and fatty acids in the coronary perfusate, the hearts of obese rats developed an increased infarct size (41.9 +/- 1.9% for obese vs. 22.9 +/- 2.3% for control, P < 0.05) and a reduced percent recovery of aortic output (4.2 +/- 4.2% for obese vs. 27.7 +/- 3.4% for controls, P < 0.05) after coronary artery occlusion and reperfusion. In the presence of insulin in the coronary perfusate, a cardioprotective effect was noted in both groups, an action that was greater in hearts from obese compared with control rats and which abolished the obesity-induced changes in infarct size (13.8 +/- 1.2% for controls vs. 21.0 +/- 1.6% for obese), and percent recovery of aortic output (60.2 +/- 4.7% for controls vs. 45.7 +/- 9.4% for obese). Fatty acids (0.7 mM, control; and 1.5 mM, obese) added to the coronary perfusate with in vivo concentrations of insulin dramatically increased infarct size (48.2 +/- 3.1% for obese, and 37.5 +/- 2.7% for control; P < 0.05 vs. without fatty acids) and decreased percent aortic output recovery (control, 10.4 +/- 5.2%, and obese 7.8 +/- 3.5%; P < 0.05 vs. without fatty acids) in both groups to similar values. In conclusion, in obesity, the impact of an increased susceptibility of the myocardium to ischemic-reperfusion injury on myocardial injury is likely to be overshadowed by the comparatively greater roles played by predicted increases in circulating insulin and fatty acids found in vivo. These data support the notion that adiposity per se is unlikely to be a valuable predictor of outcomes in ischemic-reperfusion injury.
Eugene F du Toit; Wayne Smith; Christo Muller; Hans Strijdom; Bernadette Stouthammer; Angela J Woodiwiss; Gavin R Norton; Amanda Lochner
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-03-21
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  294     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-05-07     Completed Date:  2008-06-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2336-43     Citation Subset:  IM    
Department of Biomedical Sciences, Faculty of Health Sciences, University of Stellenbosch, Tygerberg, South Africa.
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MeSH Terms
Cardiac Output
Diet / adverse effects
Disease Models, Animal
Fatty Acids, Nonesterified / blood,  metabolism*
Insulin / blood,  metabolism*
Insulin Resistance*
Myocardial Infarction / etiology*,  metabolism,  pathology,  physiopathology
Myocardial Reperfusion Injury / etiology*,  metabolism,  pathology,  physiopathology
Myocardium / metabolism*,  pathology
Norepinephrine / metabolism
Obesity / complications*,  etiology,  metabolism,  pathology,  physiopathology
Prediabetic State / complications*,  etiology,  metabolism,  pathology,  physiopathology
Rats, Wistar
Time Factors
Ventricular Remodeling
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 11061-68-0/Insulin; 51-41-2/Norepinephrine

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

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