Hall ME, Harmancey R, Stec DE. Lean heart: Role of leptin in cardiac hypertrophy and metabolism. World J Cardiol 2015; 7(9): 511-524 [PMID: 26413228 DOI: 10.4330/wjc.v7.i9.511]
Corresponding Author of This Article
David E Stec, PhD, Associate Professor, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, United States. dstec@umc.edu
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. Sep 26, 2015; 7(9): 511-524 Published online Sep 26, 2015. doi: 10.4330/wjc.v7.i9.511
Lean heart: Role of leptin in cardiac hypertrophy and metabolism
Michael E Hall, Romain Harmancey, David E Stec
Michael E Hall, Department of Medicine/Division of Cardiology, University of Mississippi Medical Center, Jackson, MS 39216, United States
Michael E Hall, Romain Harmancey, David E Stec, Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, United States
Michael E Hall, Romain Harmancey, David E Stec, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216, United States
Author contributions: All authors contributed to this manuscript.
Supported by the National Heart, Lung and Blood Institute, Nos. PO1HL-051971 and R00HL112952; and the National Institute of General Medical Sciences, No. P20GM-104357; and the American Heart Association, No. 14SDG20490339.
Conflict-of-interest statement: The authors declare no financial conflict of interest including: fees for serving as a speaker or as consultant and/or an adcisory bord member. Ownership of any stocks and/or shares or patents releted to research had ribed in this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: David E Stec, PhD, Associate Professor, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, United States. dstec@umc.edu
Telephone: +1-601-8151859 Fax: +1-601-9841817
Received: April 2, 2015 Peer-review started: April 3, 2015 First decision: June 3, 2015 Revised: June 16, 2015 Accepted: July 21, 2015 Article in press: July 23, 2015 Published online: September 26, 2015 Processing time: 170 Days and 23.9 Hours
Abstract
Leptin is an adipokine that has been linked with the cardiovascular complications resulting from obesity such as hypertension and heart disease. Obese patients have high levels of circulating leptin due to increased fat mass. Clinical and population studies have correlated high levels of circulating leptin with the development of cardiac hypertrophy in obesity. Leptin has also been demonstrated to increase the growth of cultured cardiomyocytes. However, several animal studies of obese leptin deficient mice have not supported a role for leptin in promoting cardiac hypertrophy so the role of leptin in this pathological process remains unclear. Leptin is also an important hormone in the regulation of cardiac metabolism where it supports oxidation of glucose and fatty acids. In addition, leptin plays a critical role in protecting the heart from excess lipid accumulation and the formation of toxic lipids in obesity a condition known as cardiac lipotoxicity. This paper focuses on the data supporting and refuting leptin’s role in promoting cardiac hypertrophy as well as its important role in the regulation of cardiac metabolism and protection against cardiac lipotoxicity.
Core tip: Leptin is a hormone derived from adipocytes which regulates food intake and body weight. It is present at high levels in obese individuals where it can impact organs such as the heart. Leptin has been shown to both promote and protect the heart against obesity induced heart disease. This review examines the controversial role of leptin in the development of cardiac hypertrophy as well as its important role in regulating cardiac metabolism and protecting the heart against obesity induced lipotoxicity.
