Cited by 165Cardiac Ischemia and ReperfusionCardiovascular Function and Risk FactorsPeroxisome Proliferator-Activated Receptors

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Thiazolidinedione Treatment Normalizes Insulin Resistance and Ischemic Injury in the Zucker Fatty Rat Heart

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Sidell, Robert J., Cole, Mark A., Draper, Nicholas J., Desrois, Martine, Buckingham, Robin E., Clarke, Kieran·2002·Diabetes

DOI 10.2337/diabetes.51.4.1110

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Abstract

Obesity is associated with risk factors for cardiovascular disease, including insulin resistance, and can lead to cardiac hypertrophy and congestive heart failure. Here, we used the insulin-sensitizing agent rosiglitazone to investigate the cellular mechanisms linking insulin resistance in the obese Zucker rat heart with increased susceptibility to ischemic injury. Rats were treated for 7 or 14 days with 3 mg/kg per os rosiglitazone. Hearts were isolated and perfused before and during insulin stimulation or during 32 min low-flow ischemia at 0.3 ml · min−1 · grams wet wt−1 and reperfusion. d[2-3H]glucose was used as a tracer of glucose uptake, and phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow energetics during ischemia. At 12 months of age, obese rat hearts were insulin resistant with decreased GLUT4 protein expression. During ischemia, glucose uptake was lower and depletion of ATP was greater in obese rat hearts, thereby significantly impairing recovery of contractile function during reperfusion. Rosiglitazone treatment normalized the insulin resistance and restored GLUT4 protein levels in obese rat hearts. Glucose uptake during ischemia was also normalized by rosiglitazone treatment, thereby preventing the greater loss of ATP and restoring recovery of contractile function to that of lean rat hearts. We conclude that rosiglitazone treatment, by normalizing glucose uptake, protected obese rat hearts from ischemic injury.

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Self-citation

Authors: Sidell, R. J., Cole, M. A., Draper, N. J., Desrois, M., Buckingham, R. E., & Clarke, K.
Affiliations: University of Oxford (GB)
GlaxoSmithKline (United Kingdom) (GB)
ORCID: Cole, Mark A.
Desrois, Martine
Clarke, Kieran
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2002-04-01
Volume: 51
Issue: 4
Pages: 1110-1117
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/diabetes.51.4.1110
OpenAlex: W2166216264
Cited by: 165
References: 50
Citations by year: 2026: 1 · 2025: 2 · 2022: 1 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 6 · 2016: 5 · 2015: 9 · 2014: 8 · 2013: 9 · 2012: 8
FWCI: 8.50
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Diabetes (publishedVersion)
PubMed (publishedVersion)
Funders: British Heart Foundation (PS/02/002/14893)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords: rosiglitazone, thiazolidinediones, insulin resistance, obesity, Zucker fatty rats, myocardial ischemia, myocardial ischemia-reperfusion injury, GLUT4, glucose uptake, cardiac contractile function, cardiac hypertrophy, congestive heart failure
MeSH terms: Rosiglitazone, Animals, Blood Glucose, Blood Pressure, Body Weight, Heart, Heart Rate, Hypoglycemic Agents, Insulin Resistance, Obesity, Organ Size, Perfusion, Rats, Zucker, Reference Values, Thiazoles, Time Factors, Myocardial Reperfusion, Myocardial Ischemia, Thiazolidinediones, Rats

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Thiazolidinedione Treatment Normalizes Insulin Resistance and Ischemic Injury in the Zucker Fatty Rat Heart

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