Journal
NATURE MEDICINE
Volume 10, Issue 12, Pages 1384-1389Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm1137
Keywords
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Funding
- NHLBI NIH HHS [HL20612, P01 HL066957-030004, HL61639, R01 HL061639, P01 HL066957, T32 HL007224, HL66957] Funding Source: Medline
- NIAMS NIH HHS [R01 AR040197-14, R01 AR040197, AR40197] Funding Source: Medline
- NIA NIH HHS [AG17241, R01 AG015052-02, R01 AG017241-03, R37 AG015052, R01 AG017241, AG15052, R01 AG015052] Funding Source: Medline
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Patients with diabetes and other obesity-linked conditions have increased susceptibility to cardiovascular disorders(1). The adipocytokine adiponectin is decreased in patients with obesity-linked diseases(2). 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.
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