Structural and Metabolic Effects of Obesity on the Myocardium and the Aorta

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Abstract

Obesity per se is a recognized risk factor for cardiovascular disease exerting independent adverse effects on the cardiovascular system. Despite this well documented link, the mechanisms by which obesity modulates cardiovascular risk are not well understood. Obesity is linked to a wide variety of cardiac changes, from subclinical diastolic dysfunction to end stage systolic heart failure. In addition, obesity causes changes in cardiac metabolism that make ATP production and utilization less efficient producing functional consequences that are linked to the increased rate of heart failure in this population. This review focuses on the cardiovascular structural and metabolic remodelling that occurs in obesity with and without co-morbidities and the potential links to increased mortality in this population.

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Myocardial fatty acid metabolism in health and disease.

Gary D. Lopaschuk, John Ussher, Clifford D L Folmes … (2010)

There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the beta-oxidation of long-chain fatty acids. The control of fatty acid beta-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via beta-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and beta-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid beta-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid beta-oxidation and how alterations in fatty acid beta-oxidation can contribute to heart disease. The implications of inhibiting fatty acid beta-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.

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Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old.

Kenneth F Adams, Arthur Schatzkin, Tamara Harris … (2006)

Obesity, defined by a body-mass index (BMI) (the weight in kilograms divided by the square of the height in meters) of 30.0 or more, is associated with an increased risk of death, but the relation between overweight (a BMI of 25.0 to 29.9) and the risk of death has been questioned. We prospectively examined BMI in relation to the risk of death from any cause in 527,265 U.S. men and women in the National Institutes of Health-AARP cohort who were 50 to 71 years old at enrollment in 1995-1996. BMI was calculated from self-reported weight and height. Relative risks and 95 percent confidence intervals were adjusted for age, race or ethnic group, level of education, smoking status, physical activity, and alcohol intake. We also conducted alternative analyses to address potential biases related to preexisting chronic disease and smoking status. During a maximum follow-up of 10 years through 2005, 61,317 participants (42,173 men and 19,144 women) died. Initial analyses showed an increased risk of death for the highest and lowest categories of BMI among both men and women, in all racial or ethnic groups, and at all ages. When the analysis was restricted to healthy people who had never smoked, the risk of death was associated with both overweight and obesity among men and women. In analyses of BMI during midlife (age of 50 years) among those who had never smoked, the associations became stronger, with the risk of death increasing by 20 to 40 percent among overweight persons and by two to at least three times among obese persons; the risk of death among underweight persons was attenuated. Excess body weight during midlife, including overweight, is associated with an increased risk of death. Copyright 2006 Massachusetts Medical Society.

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The mechanisms of action of PPARs.

Joel Berger, David E. Moller (2002)

The peroxisome proliferator-activated receptors (PPARs) are a group of three nuclear receptor isoforms, PPAR gamma, PPAR alpha, and PPAR delta, encoded by different genes. PPARs are ligand-regulated transcription factors that control gene expression by binding to specific response elements (PPREs) within promoters. PPARs bind as heterodimers with a retinoid X receptor and, upon binding agonist, interact with cofactors such that the rate of transcription initiation is increased. The PPARs play a critical physiological role as lipid sensors and regulators of lipid metabolism. Fatty acids and eicosanoids have been identified as natural ligands for the PPARs. More potent synthetic PPAR ligands, including the fibrates and thiazolidinediones, have proven effective in the treatment of dyslipidemia and diabetes. Use of such ligands has allowed researchers to unveil many potential roles for the PPARs in pathological states including atherosclerosis, inflammation, cancer, infertility, and demyelination. Here, we present the current state of knowledge regarding the molecular mechanisms of PPAR action and the involvement of the PPARs in the etiology and treatment of several chronic diseases.

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Author and article information

Journal

Journal ID (publisher-id): OFA

Journal ID (pmc): OFA

Journal ID (nlm-ta): Obes Facts

Journal ID (doi): 10.1159/issn.1662-4025

Title: Obesity Facts

Publisher: S. Karger AG

ISSN (Print): 1662-4025

ISSN (Electronic): 1662-4033

Publication date Subscription-year: 2014

Publication date (Print): October 2014

Publication date (Electronic): 23 October 2014

Volume: 7

Issue: 5

Pages: 329-338

Affiliations

University of Oxford Centre for Clinical Magnetic Resonance Research (OCMR), Radcliffe Department of Medicine, Division of Cardiovascular Medicine, University of Oxford, UK

Article

Publisher ID: 368429 Other ID: Obes Facts 2014;7:329-338

DOI: 10.1159/000368429

PMC ID: 5644846

PubMed ID: 25342107

SO-VID: fe9120f1-8bcb-43c6-9af3-b60b824d7fbe

License:

Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 12 August 2013

Date accepted : 08 November 2013

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Pages: 10

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Structural and Metabolic Effects of Obesity on the Myocardium and the Aorta

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Karger: Nutrition and Dietetics

Most cited references 96

Myocardial fatty acid metabolism in health and disease.

Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old.

The mechanisms of action of PPARs.

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Cited by 9

Most referenced authors 1,465