Author: ["Rei Shibata","Noriyuki Ouchi","Masahiro Ito","Shinji Kihara","Ichiro Shiojima","David R Pimentel","Masahiro Kumada","Kaori Sato","Stephan Schiekofer","Koji Ohashi","Tohru Funahashi","Wilson S Colucci","Kenneth Walsh"]
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Abstract
Patients with diabetes and other obesity-linked conditions have increased susceptibility to cardiovascular disorders1. The adipocytokine adiponectin is decreased in patients with obesity-linked diseases2. Here, we found that pressure overload in adiponectin-deficient mice resulted in enhanced concentric cardiac hypertrophy and increased mortality that was associated with increased extracellular signal-regulated kinase (ERK) and diminished AMP-activated protein kinase (AMPK) signaling in the myocardium. Adenovirus-mediated supplemention of adiponectin attenuated cardiac hypertrophy in response to pressure overload in adiponectin-deficient, wild-type and diabetic db/db mice. In cultures of cardiac myocytes, adiponectin activated AMPK and inhibited agonist-stimulated hypertrophy and ERK activation. Transduction with a dominant-negative form of AMPK reversed these effects, suggesting that adiponectin inhibits hypertrophic signaling in the myocardium through activation of AMPK signaling. Adiponectin may have utility for the treatment of hypertrophic cardiomyopathy associated with diabetes and other obesity-related diseases.Cite this article
Shibata, R., Ouchi, N., Ito, M. et al. Adiponectin-mediated modulation of hypertrophic signals in the heart. Nat Med 10, 1384–1389 (2004). https://doi.org/10.1038/nm1137 