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Cardiac dysfunction in β-carotene-15,15′-dioxygenase-deficient mice is associated with altered retinoid and lipid metabolism.
- Source :
- American Journal of Physiology: Heart & Circulatory Physiology; 12/1/2014, Vol. 307 Issue 11, pH1675-H1684, 10p
- Publication Year :
- 2014
-
Abstract
- Dietary carote-noids like β-carotene are converted within the body either to retinoid, via β-carotene-15,15′-dioxygenase (BCO1), or to β-apo-carotenoids, via β-carotene-9′,10′-oxygenase 2. Some β-apo-carotenoids are po-tent antagonists of retinoic acid receptor (RAR)-mediated transcrip-tional regulation, which is required to ensure normal heart develop-ment and functions. We established liquid chromatography tandem mass spectrometery methods for measuring concentrations of 10 β-apo-carotenoids in mouse plasma, liver, and heart and assessed how these are influenced by Bco1 deficiency and β-carotene intake. Sur-prisingly, Bco1<superscript>-/-</superscript> mice had an increase in heart levels of retinol, nonesterified fatty acids, and ceramides and a decrease in heart triglycerides. These lipid changes were accompanied by elevations in levels of genes important to retinoid metabolism, specifically retinol dehydrogenase 10 and retinol-binding protein 4, as well as genes involved in lipid metabolism, including peroxisome proliferator-acti-vated receptor-7, lipoprotein lipase, Cd36, stearoyl-CoA desaturase 1, and fatty acid synthase. We also obtained evidence of compromised heart function, as assessed by two-dimensional echocardiography, in Bco1<superscript>-/-</superscript> mice. However, the total absence of Bco1 did not substan-tially affect β-apo-carotenoid concentrations in the heart. β-Carotene administration to matched Bco1<superscript>-/-</superscript> and wild-type mice elevated total β-apo-carotenal levels in the heart, liver, and plasma and total β-apo-carotenoic acid levels in the liver. Thus, BCO1 modulates heart metabolism and function, possibly by altering levels of cofactors required for the actions of nuclear hormone receptors. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 03636135
- Volume :
- 307
- Issue :
- 11
- Database :
- Complementary Index
- Journal :
- American Journal of Physiology: Heart & Circulatory Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 99858462
- Full Text :
- https://doi.org/10.1152/ajpheart.00548.2014