Ni-Huiping Son, Tae-Sik Park, Haruyo Yamashita, Masayoshi Yokoyama, Lesley A. Huggins, Kazue Okajima, Shunichi Homma, Matthias J. Szabolcs, Li-Shin Huang, Ira J. Goldberg
J Clin Invest.
2007;
117(10):2791–2801
doi:10.1172/JCI30335
This article Copyright © 2007, The American Society for Clinical Investigation
Abstract
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T
hree forms of PPARs are expressed in the heart. In animal models, PPARγ agonist treatment improves lipotoxic cardiomyopathy; however, PPARγ agonist treatment of humans is associated with peripheral edema and increased heart failure. To directly assess effects of increased PPARγ on heart function, we created transgenic mice expressing PPARγ1 in the heart via the cardiac α–myosin heavy chain (α-MHC) promoter. PPARγ1-transgenic mice had increased cardiac expression of fatty acid oxidation genes and increased lipoprotein triglyceride (TG) uptake. Unlike in cardiac PPARα-transgenic mice, heart glucose transporter 4 (GLUT4) mRNA expression and glucose uptake were not decreased. PPARγ1-transgenic mice developed a dilated cardiomyopathy associated with increased lipid and glycogen stores, distorted architecture of the mitochondrial inner matrix, and disrupted cristae. Thus, while PPARγ agonists appear to have multiple beneficial effects, their direct actions on the myocardium have the potential to lead to deterioration in heart function.
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