title: Leptin as a cardiac pro-hypertrophic factor and its potential role in the development of heart failure.
abstract: The identification of the adipocyte as a source of production of biologically-active peptides has materialized into an active area of research related to the role of these peptides in physiology and pathophysiology. Moreover, this research has resulted in the identification of the adipocyte as an endocrine organ producing potent bioactive compounds. An increasing number of these adipokines are being identified, the first of which was leptin, a product of the obesity gene whose primary function is to act as a satiety factor but which is now known to exert a myriad of effects. It is now recognized that virtually all adipokines produce effects on numerous organ systems including the heart and many of these, including leptin, are produced by cardiac tissue. Here we focus primarily on the diverse effects of leptin on the heart especially as it pertains to hypertrophy and discuss the potential cell signaling mechanisms underlying their actions. Current evidence suggests that leptin is a cardiac hypertrophic factor and from clinical studies there is evidence that hyperleptinemia is associated with cardiovascular risk especially as it pertains to heart failure. While more substantial research needs to be carried out, leptin may represent a potential link between obesity, which is associated with hyperleptinemia, and increased cardiovascular risk.
authors.forename: Morris
authors.initials: M
authors.lastname: Karmazyn
authors.affiliation: Department of Physiology and Pharmacology, University of Western Ontario, Schulich School of Medicine and Dentistry, Medical Sciences Building, London, ON N6A 5C1, Canada. Morris.Karmazyn@Schulich.uwo.ca.
authors.forename: Venkatesh
authors.initials: V
authors.lastname: Rajapurohitam
mesh_terms: D000818:Animals; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D002319:Cardiovascular System / Q000378:metabolism*; D018450:Disease Progression; D006333:Heart Failure / Q000209:etiology*; D006801:Humans; D020738:Leptin / Q000097:blood / Q000378:metabolism*; D008955:Models, Cardiovascular; D054411:Receptors, Leptin / Q000819:agonists* / Q000378:metabolism; D015398:Signal Transduction
chemical_list: C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin