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Rosiglitazone Treatment in Zucker Diabetic Fatty Rats Is Associated With Ameliorated Cardiac Insulin Resistance and Protection From Ischemia/Reperfusion-Induced Myocardial Injury
Open accessAbstract
The mechanism responsible for the enhanced myocardial susceptibility to ischemic insult in patients with type 2 diabetes is not clear. The present study examines the effect of rosiglitazone treatment on cardiac insulin sensitization and its association with cardioprotection from ischemia/reperfusion injury in an animal model of diabetes. Male Zucker diabetic fatty (ZDF) rats were treated with rosiglitazone (3 mg · kg−1 · day−1 orally) or vehicle for 8 days before undergoing 30 min of coronary artery ligation, followed by reperfusion for 4 h (apoptosis) or 24 h (infarction). Rosiglitazone reduced the blood levels of glucose, triglycerides, and free fatty acids; enhanced cardiac glucose oxidation; and increased Akt phosphorylation (Akt-pS473) 2.1-fold and Akt kinase activity 1.8-fold in the ischemic myocardium. The phosphorylation of two downstream targets of Akt, glycogen synthase kinase-3β and FKHR (forkhead transcription factor), was also enhanced by 2- and 2.9-fold, respectively. In rosiglitazone-treated rats, the number of apoptotic cardiomyocytes and the myocardial infarct size were decreased by 58 and 46%, respectively, and the myocardial contractile dysfunction was improved. Blockade of the insulin-Akt signaling pathway by wortmannin in the 8-day rosiglitazone-treated ZDF rats resulted in a markedly diminished cardioprotective effect of rosiglitazone. In addition, 8-day rosiglitazone treatment in Zucker lean rats or 2-day rosiglitazone treatment in ZDF rats, both of which showed no change in whole-body insulin sensitivity, resulted in a significant reduction in cardiac infarct size, but to a lesser degree when compared with that observed in 8-day rosiglitazone–treated ZDF rats. These results suggest that chronic treatment with rosiglitazone protects the heart against ischemia/reperfusion injury in ZDF rats, and that the enhanced cardiac protection observed after rosiglitazone treatment might be attributable in part to an improvement in cardiac insulin sensitivity.
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“In contrast, studies in older Zucker rats demonstrated reduced recovery from ischemia, which could be prevented by treating these animals with a TZD (159, 322, 389).”
From Cardiac remodeling in obesity (2008) · cites this paper as [389]
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Metadata
- Authors
- Yue, T.-L., Bao, W., Gu, J.-L., Cui, J., Tao, L., Ma, X.-L., Ohlstein, E. H., & Jucker, B. M.
- Affiliations
- From the Department of Investigative and Cardiac Biology, GlaxoSmithKline Pharmaceuticals, King of Prussia, Pennsylvania
- GlaxoSmithKline (United States) (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-02-01
- Volume
- 54
- Issue
- 2
- Pages
- 554-562
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2154626866
- Cited by
- 170
- References
- 41
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 2 · 2017: 4 · 2016: 3 · 2015: 7 · 2014: 7 · 2013: 10 · 2012: 14
- FWCI
- 13.37
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- rosiglitazone, cardiac insulin resistance, insulin sensitization, myocardial ischemia-reperfusion injury, type 2 diabetes, Zucker diabetic fatty rats, Akt signaling, glycogen synthase kinase-3β, forkhead transcription factor, cardiomyocyte apoptosis, myocardial infarct size, myocardial contractile dysfunction, wortmannin, PPARγ agonists
- MeSH terms
- Rosiglitazone, Administration, Oral, Animals, Blood Glucose, Coronary Vessels, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Heart, Hypoglycemic Agents, Insulin Resistance, Male, Myocardial Infarction, Myocardium, Rats, Zucker, Triglycerides, Myocardial Reperfusion Injury, Thiazolidinediones, Rats
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