Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function

A.J. Bakermans; T.R. Geraedts; M. Weeghel, van; S.W. Denis; M. Jaoa Ferraz; J.M.F.G. Aerts; J. Aten; K. Nicolay; S.M. Houten; J.J. Prompers

doi:10.1161/CIRCIMAGING.111.963751

Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function

A.J. Bakermans, T.R. Geraedts, M. Weeghel, van, S.W. Denis, M. Jaoa Ferraz, J.M.F.G. Aerts, J. Aten, K. Nicolay, S.M. Houten, J.J. Prompers

Research output: Contribution to journal › Article › Academic › peer-review

49 Citations (Scopus)

Abstract

Background—Lipotoxicity may be a key contributor to the pathogenesis of cardiac abnormalities in mitochondrial long-chain fatty acid ß-oxidation (FAO) disorders. Few data are available on myocardial lipid levels and cardiac performance in FAO deficiencies. The purpose of this animal study is to assess fasting-induced changes in cardiac morphology, function, and triglyceride (TG) storage as a consequence of FAO deficiency in a noninvasive fashion. Methods and Results—MRI and proton magnetic resonance spectroscopy (1H-MRS) were applied in vivo in long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mice and wild-type (WT) mice (n=8 per genotype). Fasting was used to increase the heart's dependency on FAO for maintenance of energy homeostasis. In vivo data were complemented with ex vivo measurements of myocardial lipids. Left ventricular (LV) mass was higher in LCAD KO mice compared with WT mice (P

Original language	English
Pages (from-to)	558-565
Journal	Circulation. Cardiovascular Imaging
Volume	4
Issue number	5
DOIs	https://doi.org/10.1161/CIRCIMAGING.111.963751
Publication status	Published - 2011

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Bakermans, A. J., Geraedts, T. R., Weeghel, van, M., Denis, S. W., Jaoa Ferraz, M., Aerts, J. M. F. G., Aten, J., Nicolay, K., Houten, S. M., & Prompers, J. J. (2011). Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function. Circulation. Cardiovascular Imaging, 4(5), 558-565. https://doi.org/10.1161/CIRCIMAGING.111.963751

Bakermans, A.J. ; Geraedts, T.R. ; Weeghel, van, M. ; Denis, S.W. ; Jaoa Ferraz, M. ; Aerts, J.M.F.G. ; Aten, J. ; Nicolay, K. ; Houten, S.M. ; Prompers, J.J. / Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function. In: Circulation. Cardiovascular Imaging. 2011 ; Vol. 4, No. 5. pp. 558-565.

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title = "Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function",

abstract = "Background—Lipotoxicity may be a key contributor to the pathogenesis of cardiac abnormalities in mitochondrial long-chain fatty acid {\ss}-oxidation (FAO) disorders. Few data are available on myocardial lipid levels and cardiac performance in FAO deficiencies. The purpose of this animal study is to assess fasting-induced changes in cardiac morphology, function, and triglyceride (TG) storage as a consequence of FAO deficiency in a noninvasive fashion. Methods and Results—MRI and proton magnetic resonance spectroscopy (1H-MRS) were applied in vivo in long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mice and wild-type (WT) mice (n=8 per genotype). Fasting was used to increase the heart's dependency on FAO for maintenance of energy homeostasis. In vivo data were complemented with ex vivo measurements of myocardial lipids. Left ventricular (LV) mass was higher in LCAD KO mice compared with WT mice (P",

author = "A.J. Bakermans and T.R. Geraedts and {Weeghel, van}, M. and S.W. Denis and {Jaoa Ferraz}, M. and J.M.F.G. Aerts and J. Aten and K. Nicolay and S.M. Houten and J.J. Prompers",

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doi = "10.1161/CIRCIMAGING.111.963751",

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Bakermans, AJ , Geraedts, TR, Weeghel, van, M, Denis, SW, Jaoa Ferraz, M, Aerts, JMFG, Aten, J, Nicolay, K, Houten, SM & Prompers, JJ 2011, 'Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function', Circulation. Cardiovascular Imaging, vol. 4, no. 5, pp. 558-565. https://doi.org/10.1161/CIRCIMAGING.111.963751

Fasting-induced myocardial lipid accumulation in long-chain acyl-CoA dehydrogenase knockout mice is accompanied by impaired left ventricular function. / Bakermans, A.J.; Geraedts, T.R.; Weeghel, van, M.; Denis, S.W.; Jaoa Ferraz, M.; Aerts, J.M.F.G.; Aten, J.; Nicolay, K.; Houten, S.M.; Prompers, J.J.

In: Circulation. Cardiovascular Imaging, Vol. 4, No. 5, 2011, p. 558-565.

Research output: Contribution to journal › Article › Academic › peer-review

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AU - Bakermans, A.J.

AU - Geraedts, T.R.

AU - Weeghel, van, M.

AU - Denis, S.W.

AU - Jaoa Ferraz, M.

AU - Aerts, J.M.F.G.

AU - Aten, J.

AU - Nicolay, K.

AU - Houten, S.M.

AU - Prompers, J.J.

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AB - Background—Lipotoxicity may be a key contributor to the pathogenesis of cardiac abnormalities in mitochondrial long-chain fatty acid ß-oxidation (FAO) disorders. Few data are available on myocardial lipid levels and cardiac performance in FAO deficiencies. The purpose of this animal study is to assess fasting-induced changes in cardiac morphology, function, and triglyceride (TG) storage as a consequence of FAO deficiency in a noninvasive fashion. Methods and Results—MRI and proton magnetic resonance spectroscopy (1H-MRS) were applied in vivo in long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mice and wild-type (WT) mice (n=8 per genotype). Fasting was used to increase the heart's dependency on FAO for maintenance of energy homeostasis. In vivo data were complemented with ex vivo measurements of myocardial lipids. Left ventricular (LV) mass was higher in LCAD KO mice compared with WT mice (P

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