| Bariatric surgery to unload the stressed heart: a metabolic hypothesis. | |
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MedLine Citation:
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PMID: 22307676 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Obesity is an independent risk factor for cardiovascular disease. Data from the Framingham Study have reported a higher incidence of heart failure in obese individuals compared with a normal cohort. The body initially copes with the abundance of fuel present in an obese milieu by storing it in adipose tissue. However, when the storage capacity is exceeded, the excess energy is taken up and stored ectopically as fat in vital organs such as the heart. Indeed, intramyocardial lipid overload is present in hearts of obese patients, as well as in hearts of animal models of obesity, and is associated with a distinct gene expression profile and cardiac dysfunction. By imposing a metabolic stress on the heart, obesity causes it to hypertrophy and ultimately to fail. Conventional measures to treat obesity include diet, exercise, and drugs. More recently, weight loss surgery (WLS) has achieved increasing prominence because of its ability to reduce the neurohumoral load, normalize metabolic dysregulation, and improve overall survival. The effects of WLS on systemic metabolic, neurohumoral, and hemodynamic parameters are well described and include an early normalization of serum glucose and insulin levels as well as reduction in blood pressure. WLS is also associated with reverse cardiac remodeling, regression of left ventricular hypertrophy, and improved left ventricular and right ventricular function. By targeting the source of the excess energy, we hypothesize that WLS improves contractile function by limiting exogenous substrate availability to the metabolically overloaded heart. These changes have also been found to be associated with increased levels of adiponectin and improved insulin sensitivity. Taken together, the sustained beneficial effects of WLS on left ventricular mass and function highlight the need to better understand the mechanism by which obesity regulates cardiovascular physiology. |
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Authors:
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Mohamed F Algahim; Shiraj Sen; Heinrich Taegtmeyer |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2012-02-03 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 302 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-04-16 Completed Date: 2012-05-30 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1539-45 Citation Subset: IM |
Affiliation:
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Division of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas 77030, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bariatric Surgery* Energy Metabolism / physiology Heart / physiology* Homeostasis / physiology Myocardium / metabolism Obesity / physiopathology Weight Loss / physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL073162/HL/NHLBI NIH HHS; R01-HL-073162/HL/NHLBI NIH HHS; R01-HL-61483/HL/NHLBI NIH HHS; T32//PHS HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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