ArticleJournal of biomedical science2009
Impairment of insulin-stimulated Akt/GLUT4 signaling is associated with cardiac contractile dysfunction and aggravates I/R injury in STZ-diabetic rats.
Article in Journal of biomedical science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
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- Treatment with crocin attenuates cardiac metabolic disturbances and subsequent inflammation in streptozotocin-induced diabetes.Molecular and cellular biochemistry · 2025Article
- Post-translational modifications in diabetic cardiomyopathy.Journal of cellular and molecular medicine · 2024Review
- The SWGEDWGEIW from Soybean Peptides Reduces Insulin Resistance in 3T3-L1 Adipocytes by Activating p-Akt/GLUT4 Signaling Pathway.Molecules (Basel, Switzerland) · 2023Article
- Lipophilic and Hydrophilic Compounds fromLife (Basel, Switzerland) · 2022Review
- Genetic analyses of the electrocardiographic QT interval and its components identify additional loci and pathways.Nature communications · 2022Article
- New insights into the role of melatonin in diabetic cardiomyopathy.Pharmacology research & perspectives · 2022Review
- Article
- Hesperidin ameliorates signs of the metabolic syndrome and cardiac dysfunction via IRS/Akt/GLUT4 signaling pathway in a rat model of diet-induced metabolic syndrome.European journal of nutrition · 2021Article
- Human-induced pluripotent stem cells for modelling metabolic perturbations and impaired bioenergetics underlying cardiomyopathies.Cardiovascular research · 2021Review
- DRD4 Mitigates Myocardial Ischemia/Reperfusion Injury in Association With PI3K/AKT Mediated Glucose Metabolism.Frontiers in pharmacology · 2020Article
- Palmitic acid is an intracellular signaling molecule involved in disease development.Cellular and molecular life sciences : CMLS · 2019Review
- Carvacrol Attenuates Diabetic Cardiomyopathy by Modulating the PI3K/AKT/GLUT4 Pathway in Diabetic Mice.Frontiers in pharmacology · 2019Article
- Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function.Circulation research · 2016Article
- Article
- Diabetes Alters the Expression and Translocation of the Insulin-Sensitive Glucose Transporters 4 and 8 in the Atria.PloS one · 2015Article
- Coefficient of glucose variation is independently associated with mortality in critically ill patients receiving intravenous insulin.Critical care (London, England) · 2014Article
- Chicken embryos as a potential new model for early onset type I diabetes.Journal of diabetes research · 2014Article
- Article
- Myocardial AKT: the omnipresent nexus.Physiological reviews · 2011Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we established systemic in-vivo evidence from molecular to organism level to explain how diabetes can aggravate myocardial ischemia-reperfusion (I/R) injury and revealed the role of insulin signaling (with specific focus on Akt/GLUT4 signaling molecules). The myocardial I/R injury was induced by the left main coronary artery occlusion for 1 hr and then 3 hr reperfusion in control, streptozotocin (STZ)-induced insulinopenic diabetes, and insulin-treated diabetic rats. The diabetic rats showed a significant decrease in heart rate, and a prolonged isovolumic relaxation (tau) which lead to decrease in cardiac output (CO) without changing total peripheral resistance (TPR). The phosphorylated Akt and glucose transporter 4 (GLUT 4) protein levels were dramatically reduced in both I/R and non-I/R diabetic rat hearts. Insulin treatment in diabetes showed improvement of contractile function as well as partially increased Akt phosphorylation and GLUT 4 protein levels. In the animals subjected to I/R, the mortality rates were 25%, 65%, and 33% in the control, diabetic, and insulin-treated diabetic group respectively. The I/R-induced arrhythmias and myocardial infarction did not differ significantly between the control and the diabetic groups. Consistent with its anti-hyperglycemic effects, insulin significantly reduced I/R-induced arrhythmias but had no effect on I/R-induced infarctions. Diabetic rat with I/R exhibited the worse hemodynamic outcome, which included systolic and diastolic dysfunctions. Insulin treatment only partially improved diastolic functions and elevated P-Akt and GLUT 4 protein levels. Our results indicate that cardiac contractile dysfunction caused by a defect in insulin-stimulated Akt/GLUT4 may be a major reason for the high mortality rate in I/R injured diabetic rats.
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