Document Detail

Bariatric surgery to unload the stressed heart: a metabolic hypothesis.
MedLine Citation:
PMID:  22307676     Owner:  NLM     Status:  MEDLINE    
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.
Mohamed F Algahim; Shiraj Sen; Heinrich Taegtmeyer
Related Documents :
11020156 - Model of chronic systolic and diastolic dysfunction after cryothermia-induced myocardia...
2345236 - Diastolic function in patients undergoing coronary angioplasty: influence of degree of ...
22710146 - External validation of the grace freedom from events score.
1750536 - Coronary artery narrowing in rats: mechanical alterations of left and right myocardium.
17243506 - Significance of brain natriuretic peptide in the evaluation of symptoms and the degree ...
10475726 - An acute ischaemic event associated with the use of venlafaxine: a case report and prop...
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    
Division of Cardiology, Department of Internal Medicine, University of Texas Medical School at Houston, Houston, Texas 77030, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Bariatric Surgery*
Energy Metabolism / physiology
Heart / physiology*
Homeostasis / physiology
Myocardium / metabolism
Obesity / physiopathology
Weight Loss / physiology
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Vena cava and aortic smooth muscle cells express transglutaminases 1 and 4 in addition to transgluta...
Next Document:  11,12,20-Trihydroxy-eicosa-8(Z)-enoic acid: a selective inhibitor of 11,12-EET-induced relaxations o...