Document Detail


Bariatric surgery to unload the stressed heart: a metabolic hypothesis.
MedLine Citation:
PMID:  22307676     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Mohamed F Algahim; Shiraj Sen; Heinrich Taegtmeyer
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2012-02-03
Journal Detail:
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:
Created Date:  2012-04-16     Completed Date:  2012-05-30     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1539-45     Citation Subset:  IM    
Affiliation:
Division of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bariatric Surgery*
Energy Metabolism / physiology
Heart / physiology*
Homeostasis / physiology
Myocardium / metabolism
Obesity / physiopathology
Weight Loss / physiology
Grant Support
ID/Acronym/Agency:
R01 HL073162/HL/NHLBI NIH HHS; R01-HL-073162/HL/NHLBI NIH HHS; R01-HL-61483/HL/NHLBI NIH HHS; T32//PHS HHS
Comments/Corrections

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