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Circ Res. 2009 Aug 14;105(4):326-34. doi: 10.1161/CIRCRESAHA.109.200501. Epub 2009 Jul 16.

Adipocyte fatty acid-binding protein suppresses cardiomyocyte contraction: a new link between obesity and heart disease.

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  • 1Medical Clinic III, Dresden University of Technology, Fetscherstr. 74, 01307 Dresden, Germany. Valeria.Zepter@uniklinikum-dresden.de

Abstract

RATIONALE:

Adipocyte fatty acid-binding protein (FABP4) is a member of the intracellular lipid-binding protein family and is predominantly expressed in adipose tissue. Emerging evidence suggests that FABP4 plays a role in some aspects of the metabolic syndrome including the development of type 2 diabetes and atherosclerosis. We have recently reported that secretory products from human adipocytes directly and acutely depressed cardiac contractile function.

OBJECTIVE:

The purpose of this study was to identify this adipocyte-derived cardiodepressant factor.

METHODS AND RESULTS:

Through mass spectrometry and immunoblotting, we have identified this cardiodepressant factor as FABP4. FABP4 represents 1.8% to 8.1% of total protein secreted by adipocytes in extracellular medium. FABP4 acutely depressed shortening amplitude as well as intracellular systolic peak Ca(2+) in a dose-dependent manner in isolated rat cardiomyocytes. Heart-specific FABP isoform (FABP3) revealed a similar cardiodepressant effect. The N-terminal amino acids 1 to 20 of FABP4 could be identified as the most effective cardiodepressive domain. We could exclude any effect of FABP4 on action potential duration and L-type Ca(2+) current, suggesting a reduced excitation-contraction gain caused by FABP4 as the main inhibitory mechanism.

CONCLUSION:

We conclude that the release of FABP4 from adipocytes may be involved in the development of cardiac contractile dysfunction of obese subjects.

PMID:
19608978
[PubMed - indexed for MEDLINE]
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