Cited by 38Cardiac Ischemia and ReperfusionCardiovascular Function and Risk FactorsAcute Myocardial Infarction Research

Size of myocardial infarction induced by ischaemia/reperfusion is unaltered in rats with metabolic syndrome

Thim, Troels, Bentzon, Jacob F., Kristiansen, Steen B., Simonsen, Ulf, Andersen, Heidi L., Wassermann, Karsten, Falk, Erling·2006·Clinical Science

Abstract

Obesity is associated with metabolic syndrome and increased incidence of and mortality from myocardial infarction. The aim of the present study was to develop an animal model with metabolic syndrome and examine how that influences size of myocardial infarcts induced by occlusion and reperfusion of the left anterior descending coronary artery. Sprague–Dawley rats (n=105) were fed either LF (low-fat) or MHF (moderately high-fat) diets for 13 weeks before coronary occlusion for 45 min, followed by reperfusion for 60 min. Compared with LF-fed and lean MHF-fed rats, obese MHF-fed rats developed metabolic disturbances similar to those seen in the metabolic syndrome, including being overweight by 24% (compared with lean MHF-fed rats), having 74% more visceral fat (compared with LF-fed rats), 15% higher blood pressure (compared with LF-fed rats), 116% higher plasma insulin (compared with lean MHF-fed rats), 10% higher fasting plasma glucose (compared with LF-fed rats), 35% higher non-fasting plasma glucose (compared with lean MHF-fed rats), 36% higher plasma leptin (compared with lean MHF-fed rats) and a tendency to lower plasma adiponectin and higher plasma non-esterified fatty acids. Infarct size was similar in the three groups of rats (36±14, 42±18 and 41±14% in obese MHF-fed, lean MHF-fed and LF-fed rats respectively). In conclusion, rats fed a MHF diet developed metabolic syndrome, but this did not influence myocardial infarct size.

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Crossref · 10.1042/cs20050326

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  • Infarct size is unchanged in high-fat fed models but increased in db/db mice.

    “Infarct size is unchanged in high-fat fed models (347) but increased in db/db mice (160).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [347]

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References 36 · Cited by 38

Authors
Thim, T., Bentzon, J. F., Kristiansen, S. B., Simonsen, U., Andersen, H. L., Wassermann, K., & Falk, E.
Affiliations
Aarhus University Hospital (DK)
Venue
Clinical Science
Published
2006-05-15
Volume
110
Issue
6
Pages
665-671
ISSN
  • 0143-5221 (ISSN-L)
  • 1470-8736
OpenAlex
W2060444942
Cited by
38
References
36
Citations by year
2025: 2 · 2024: 1 · 2022: 1 · 2020: 1 · 2017: 1 · 2014: 3 · 2013: 2 · 2012: 4
FWCI
2.80
Type
journal article
Language
en
Open access
closed
Locations
  • Clinical Science (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
Keywords
metabolic syndrome, myocardial infarction, infarct size, ischaemia-reperfusion, obesity, high-fat diet, coronary artery occlusion, visceral fat, insulin resistance, leptin, adiponectin, free fatty acids, animal models
MeSH terms
Animals, Blood Glucose, Cholesterol, Fatty Acids, Nonesterified, Insulin, Male, Myocardial Infarction, Myocardium, Myocardial Reperfusion Injury, Rats, Sprague-Dawley, Leptin, Models, Animal, Metabolic Syndrome, Rats, Adiponectin

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