This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dyck, J. R.B. Search for Related Content PubMed PubMed Citation Articles by Dyck, J. R.B. Related Collections Animal models of human disease Acute myocardial infarction

(Circulation. 2007;116:2779-2781.)
© 2007 American Heart Association, Inc.

Editorial

The Ischemic Heart

Starving to Stimulate the Adiponectin-AMPK Signaling Axis

Jason R.B. Dyck, PhD

From the Cardiovascular Research Group, Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.

Correspondence to Jason R.B. Dyck, 474 Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, Canada, T6G 2S2. E-mail jason.dyck@ualberta.ca

Key Words: Editorials • adiponectin • AMP-activated protein kinase • diet • ischemia • metabolism

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Caloric restriction has emerged as an effective strategy for lengthening lifespan in a variety of species.¹ In mammals, one mechanism for this phenomenon may be the prevention of detrimental age-related alterations in cellular function¹ and presumably subsequent improvement in organ function. The effects of caloric restriction on the heart, at least in rats and mice, involve a number of changes in gene expression that are beneficial to the aged cardiomyocyte² and/or protect the heart from ischemic injury.³ Although it is likely that all of the beneficial mediators of caloric restriction have not been identified, a number of proteins in the mammalian sirtuin family may play key roles in the regulation of health and longevity.⁴ In addition, recent evidence has suggested that alterations in whole-body energy metabolism contribute to the beneficial effects of caloric restriction.⁵ Indeed, caloric restriction in mammals leads to loss of adipose tissue and dramatically alters the action of this endocrine organ.⁶ As such, caloric restriction contributes to changes in adipose tissue–derived hormone (adipokine) secretion, which can govern whole-body metabolism.⁷ Furthermore, studies using isolated cardiac myocytes suggest that these adipokines may exert direct end-organ effects that are independent from alterations in whole-body metabolism.^8–10 One adipokine that is significantly increased during caloric restriction is adiponectin.¹¹ Previous work has shown that adiponectin exerts a host of protective effects on the cardiovascular system¹² and as such may be an essential component mediating the effects of caloric restriction.

Article p 2809

The focus on adiponectin in the cardiovascular system has been due . . . [Full Text of this Article]

This article has been cited by other articles:

				P. Iozzo, R. Lautamaki, R. Borra, H.-R. Lehto, M. Bucci, A. Viljanen, J. Parkka, V. Lepomaki, R. Maggio, R. Parkkola, et al. Contribution of Glucose Tolerance and Gender to Cardiac Adiposity J. Clin. Endocrinol. Metab., November 1, 2009; 94(11): 4472 - 4482. [Abstract] [Full Text] [PDF]

				Y. Wang, L. Tao, Y. Yuan, W. B. Lau, R. Li, B. L. Lopez, T. A. Christopher, R. Tian, and X.-L. Ma Cardioprotective effect of adiponectin is partially mediated by its AMPK-independent antinitrative action Am J Physiol Endocrinol Metab, August 1, 2009; 297(2): E384 - E391. [Abstract] [Full Text] [PDF]

				Y. Wang, E. Gao, L. Tao, W. B. Lau, Y. Yuan, B. J. Goldstein, B. L. Lopez, T. A. Christopher, R. Tian, W. Koch, et al. AMP-Activated Protein Kinase Deficiency Enhances Myocardial Ischemia/Reperfusion Injury but Has Minimal Effect on the Antioxidant/Antinitrative Protection of Adiponectin Circulation, February 17, 2009; 119(6): 835 - 844. [Abstract] [Full Text] [PDF]