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• W2100048686 abstract "HomeCirculationVol. 109, No. 7Role of Leptin in the Development of Cardiac Hypertrophy in Experimental Animals and Humans Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBRole of Leptin in the Development of Cardiac Hypertrophy in Experimental Animals and Humans Nicholas A. Tritos, Warren J. Manning and Peter G. Danias Nicholas A. TritosNicholas A. Tritos Beth Israel Deaconess Medical Center and, Harvard Medical School, Boston, Mass Search for more papers by this author , Warren J. ManningWarren J. Manning Beth Israel Deaconess Medical Center and, Harvard Medical School, Boston, Mass Search for more papers by this author and Peter G. DaniasPeter G. Danias Beth Israel Deaconess Medical Center and, Harvard Medical School, Boston, Mass Search for more papers by this author Originally published24 Feb 2004https://doi.org/10.1161/01.CIR.0000116424.65485.67Circulation. 2004;109:e67To the Editor:Barouch et al1 recently published a well-designed study demonstrating that left ventricular hypertrophy (LVH) occurs in mice that are either leptin-deficient (ob/ob) or leptin-resistant (db/db). They also found that systemic administration of leptin to the leptin-deficient animals attenuated LVH more than would be predicted by the leptin-induced hypophagia and weight loss. These observations suggest that leptin may have a direct inhibitory effect on cardiac hypertrophy.1We have recently examined the association between systemic leptin levels and cardiovascular indexes in a population of healthy obese and lean men.2,3 In addition to showing that the obese had greater absolute and height-indexed left ventricular (LV) mass (confirming the association between obesity and LVH in this normotensive population2–4), we also found a positive association between serum leptin and height-indexed LV mass,2 which did not persist after adjustment for body mass index.2The data by Barouch et al1 in experimental animals corroborate our observations in humans2,3 and provide a potential pathophysiological explanation. With rare exceptions, human obesity is associated with hyperleptinemia and apparent leptin resistance.5 LVH in this group of patients could be due to the lack of the leptin attenuating effect on LV mass, similar to the occurrence of LVH in the hyperleptinemic, leptin-resistant db/db mice. It remains to be established whether pharmacological amelioration of leptin resistance will either prevent or, at least, attenuate LVH in rodent and human obesity. References 1 Barouch LA, Berkowitz DE, Harrison RW, et al. Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice. Circulation. 2003; 108: 754–759.LinkGoogle Scholar2 Tritos NA, Kissinger KV, Manning WJ, et al. Association between ghrelin and cardiovascular indexes in healthy obese and lean men. Clin Endocrinol. 2004; 60: 60–66.CrossrefMedlineGoogle Scholar3 Danias PG, Tritos NA, Stuber M, et al. Cardiac structure and function in the obese: a cardiovascular magnetic resonance imaging study. J Cardiovasc Magn Reson. 2003; 5: 431–438.CrossrefMedlineGoogle Scholar4 Alpert MA, Terry BE, Mulekar M, et al. Cardiac morphology and left ventricular function in normotensive morbidly obese patients with and without congestive heart failure, and effect of weight loss. Am J Cardiol. 1997; 80: 736–740.CrossrefMedlineGoogle Scholar5 Flier JS. Clinical review 94: what’s in a name? In search of leptin’s physiologic role. J Clin Endocrinol Metab. 1998; 83: 1407–1413.MedlineGoogle ScholarcirculationahaCirculationCirculationCirculation0009-73221524-4539Lippincott Williams & WilkinsResponseBarouch Lili A., , Berkowitz Dan E., , Harrison Robert W., , O’Donnell Christopher P., , and Hare Joshua M., 24022004Drs Tritos, Manning, and Danias raise the important issue of clinical relevance of left ventricular hypertrophy (LVH) in mice lacking the leptin receptor (db/db) or in mice lacking leptin itself (ob/ob), both of which exhibit morbid obesity. Human obesity is largely associated with leptin resistance and elevated leptin levels, and these investigators have demonstrated a positive correlation between leptin levels and LVH in obese subjects. Importantly, leptin levels are also elevated in chronic heart failure1 and chronic hypertension,2 suggesting the presence of leptin resistance in these disorders.Indeed, we demonstrated reduction in LVH with leptin repletion in ob/ob mice, a model that can be considered analogous to reversing leptin resistance,3 as these mice have leptin receptors and presumably intact downstream signaling mechanisms. Interestingly, studies conducted in healthy individuals, free of cardiovascular disease and/or obesity, demonstrate inverse relationships between leptin levels and left ventricular mass index,4 suggesting that the primary impact of leptin is antihypertrophic when the signaling pathway is intact.These studies considered together strongly support the notion that physiological leptin signaling has homeostatic cardiovascular activity. States of LVH—both obesity and other causes of heart failure—are states of leptin resistance and are therefore marked by elevated leptin levels. Thus, it will be essential to focus research efforts on the causes of leptin resistance and determination of whether heart failure and obesity have common leptin pathway signaling abnormalities. The totality of evidence further suggests that leptin-based interventions to reduce LVH will need to address the underlying causes of leptin resistance. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Alves da Silva F, Freire L, Lima T, Santos S, Lemes S, Gai B, Colodel E, Avila E, Damazo A, Pereira M and Kawashita N (2022) Introduction of high-fat and very-high-fat diets associated with fructose drink in critical development periods causes cardiovascular damage in rats at the beginning of adult life, Nutrition, 10.1016/j.nut.2022.111689, 101, (111689), Online publication date: 1-Sep-2022. Fontes-Carvalho R, Pimenta J, Bettencourt P, Leite-Moreira A and Azevedo A (2015) Association between plasma leptin and adiponectin levels and diastolic function in the general population, Expert Opinion on Therapeutic Targets, 10.1517/14728222.2015.1019468, 19:10, (1283-1291), Online publication date: 3-Oct-2015. Kontaridis M, Geladari E and Geladari C (2015) Pathways to Myocardial Hypertrophy Introduction to Translational Cardiovascular Research, 10.1007/978-3-319-08798-6_10, (167-186), . Kshatriya S, Liu K, Salah A, Szombathy T, Freeman R, Reams G, Spear R and Villarreal D (2011) Obesity Hypertension: The Regulatory Role of Leptin, International Journal of Hypertension, 10.4061/2011/270624, 2011, (1-8), . Kshatriya S, Kozman H, Siddiqui D, Bhatta L, Liu K, Salah A, Ford T, Michiel R, Carhart R and Villarreal D (2011) Obesity–Hypertension: Leptin as the Common Link to Cardiovascular and Renal Dysregulation Molecular Defects in Cardiovascular Disease, 10.1007/978-1-4419-7130-2_25, (343-351), . Kshatriya S, Reams G, Spear R, Freeman R, Dietz J and Villarreal D (2010) Obesity hypertension: the emerging role of leptin in renal and cardiovascular dyshomeostasis, Current Opinion in Nephrology and Hypertension, 10.1097/MNH.0b013e328332fb49, 19:1, (72-78), Online publication date: 1-Jan-2010. Patel S, Reams G, Spear R, Freeman R and Villarreal D (2008) Leptin: Linking obesity, the metabolic syndrome, and cardiovascular disease, Current Hypertension Reports, 10.1007/s11906-008-0025-y, 10:2, (131-137), Online publication date: 1-Apr-2008. Mathew B, Patel S, Spear R, Villarreal D, Reams G and Freeman R (2007) Obesity-Hypertension: Emerging Concepts in Pathophysiology and Treatment, The American Journal of the Medical Sciences, 10.1097/MAJ.0b013e3180959e4e, 334:1, (23-30), Online publication date: 1-Jul-2007. Schulze P and Kratzsch J (2005) Leptin as a new diagnostic tool in chronic heart failure, Clinica Chimica Acta, 10.1016/j.cccn.2005.05.019, 362:1-2, (1-11), Online publication date: 1-Dec-2005. Przyklenk K, Maynard M, Darling C and Whittaker P (2005) Pretreatment with d- myo -Inositol Trisphosphate Reduces Infarct Size in Rabbit Hearts: Role of Inositol Trisphosphate Receptors and Gap Junctions in Triggering Protection , Journal of Pharmacology and Experimental Therapeutics, 10.1124/jpet.105.087742, 314:3, (1386-1392), Online publication date: 1-Sep-2005. February 24, 2004Vol 109, Issue 7 Advertisement Article InformationMetrics https://doi.org/10.1161/01.CIR.0000116424.65485.67PMID: 14981017 Originally publishedFebruary 24, 2004 PDF download Advertisement" @default.
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