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Isolated perfused hearts from type 2 diabetic (db/db) mice show impaired ventricular function, as well as altered cardiac metabolism. Assessment of the relationship between myocardial oxygen consumption (MVO(2)) and ventricular pressure-volume area (PVA) has also demonstrated reduced cardiac efficiency in db/db hearts. We hypothesized that lowering the plasma fatty acid supply and subsequent normalization of altered cardiac metabolism by chronic treatment with a peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist will improve cardiac efficiency in db/db hearts. Rosiglitazone (23 mg/kg body weight/day) was administered as a food admixture to db/db mice for five weeks. Ventricular function and PVA were assessed using a miniaturized (1.4 Fr) pressure-volume catheter; MVO(2) was measured using a fibre-optic oxygen sensor. Chronic rosiglitazone treatment of db/db mice normalized plasma glucose and lipid concentrations, restored rates of cardiac glucose and fatty acid oxidation, and improved cardiac efficiency. The improved cardiac efficiency was due to a significant decrease in unloaded MVO(2), while contractile efficiency was unchanged. Rosiglitazone treatment also improved functional recovery after low-flow ischemia. In conclusion, the present study demonstrates that in vivo PPARgamma-treatment restores cardiac efficiency and improves ventricular function in perfused hearts from type 2 diabetic mice.

Original publication




Journal article


Arch Physiol Biochem

Publication Date





211 - 220


Animals, Blood Glucose, Body Weight, Cardiovascular Physiological Phenomena, Coronary Vessels, Diabetes Mellitus, Type 2, Female, Heart, Ion Channels, Ischemia, Lipid Metabolism, Male, Mice, Mice, Inbred C57BL, Mitochondrial Proteins, Organ Size, Oxidation-Reduction, Oxygen Consumption, RNA, Messenger, Reperfusion Injury, Rosiglitazone, Thiazolidinediones, Uncoupling Protein 3, Ventricular Function