Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.

<h4>Aims</h4>Development of metabolic syndrome is associated with impaired cardiac performance, mitochondrial dysfunction and pro-inflammatory cytokine increase, such as the macrophage migration inhibitory factor MIF. Depending on conditions, MIF may exert both beneficial and deleterious...

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Autores principales:	Aurore Palud, Camille Marciniak, David Montaigne, Xavier Marechal, Caroline Ballot, Sidi Mohamed Hassoun, Brigitte Decoster, Remi Neviere, Steve Lancel
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f9145e85bd9e4e9fa7b5c6f95506b35f
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spelling	oai:doaj.org-article:f9145e85bd9e4e9fa7b5c6f95506b35f2021-11-18T07:53:57ZMacrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.1932-620310.1371/journal.pone.0058718https://doaj.org/article/f9145e85bd9e4e9fa7b5c6f95506b35f2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23536817/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aims</h4>Development of metabolic syndrome is associated with impaired cardiac performance, mitochondrial dysfunction and pro-inflammatory cytokine increase, such as the macrophage migration inhibitory factor MIF. Depending on conditions, MIF may exert both beneficial and deleterious effects on the myocardium. Therefore, we tested whether pharmacological inhibition of MIF prevented or worsened metabolic syndrome-induced myocardial dysfunction.<h4>Methods and results</h4>C57BL/6J mice were fed for ten weeks with 60% fat-enriched diet (HFD) or normal diet (ND). MIF inhibition was obtained by injecting mice twice a week with ISO-1, for three consecutive weeks. Then, triglycerides, cholesterol, fat mass, glucose intolerance, insulin resistance, ex vivo cardiac contractility, animal energetic substrate utilization assessed by indirect calorimetry and mitochondrial respiration and biogenesis were evaluated. HFD led to fat mass increase, dyslipidemia, glucose intolerance and insulin resistance. ISO-1 did not alter these parameters. However, MIF inhibition was responsible for HFD-induced cardiac dysfunction worsening. Mouse capacity to increase oxygen consumption in response to exercise was reduced in HFD compared to ND, and further diminished in ISO-1-treated HFD group. Mitochondrial respiration was reduced in HFD mice, treated or not with ISO-1. Compared to ND, mitochondrial biogenesis signaling was upregulated in the HFD as demonstrated by mitochondrial DNA amount and PGC-1α expression. However, this increase in biogenesis was blocked by ISO-1 treatment.<h4>Conclusion</h4>MIF inhibition achieved by ISO-1 was responsible for a reduction in HFD-induced mitochondrial biogenesis signaling that could explain majored cardiac dysfunction observed in HFD mice treated with MIF inhibitor.Aurore PaludCamille MarciniakDavid MontaigneXavier MarechalCaroline BallotSidi Mohamed HassounBrigitte DecosterRemi NeviereSteve LancelPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 3, p e58718 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Aurore Palud Camille Marciniak David Montaigne Xavier Marechal Caroline Ballot Sidi Mohamed Hassoun Brigitte Decoster Remi Neviere Steve Lancel Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
description	<h4>Aims</h4>Development of metabolic syndrome is associated with impaired cardiac performance, mitochondrial dysfunction and pro-inflammatory cytokine increase, such as the macrophage migration inhibitory factor MIF. Depending on conditions, MIF may exert both beneficial and deleterious effects on the myocardium. Therefore, we tested whether pharmacological inhibition of MIF prevented or worsened metabolic syndrome-induced myocardial dysfunction.<h4>Methods and results</h4>C57BL/6J mice were fed for ten weeks with 60% fat-enriched diet (HFD) or normal diet (ND). MIF inhibition was obtained by injecting mice twice a week with ISO-1, for three consecutive weeks. Then, triglycerides, cholesterol, fat mass, glucose intolerance, insulin resistance, ex vivo cardiac contractility, animal energetic substrate utilization assessed by indirect calorimetry and mitochondrial respiration and biogenesis were evaluated. HFD led to fat mass increase, dyslipidemia, glucose intolerance and insulin resistance. ISO-1 did not alter these parameters. However, MIF inhibition was responsible for HFD-induced cardiac dysfunction worsening. Mouse capacity to increase oxygen consumption in response to exercise was reduced in HFD compared to ND, and further diminished in ISO-1-treated HFD group. Mitochondrial respiration was reduced in HFD mice, treated or not with ISO-1. Compared to ND, mitochondrial biogenesis signaling was upregulated in the HFD as demonstrated by mitochondrial DNA amount and PGC-1α expression. However, this increase in biogenesis was blocked by ISO-1 treatment.<h4>Conclusion</h4>MIF inhibition achieved by ISO-1 was responsible for a reduction in HFD-induced mitochondrial biogenesis signaling that could explain majored cardiac dysfunction observed in HFD mice treated with MIF inhibitor.
format	article
author	Aurore Palud Camille Marciniak David Montaigne Xavier Marechal Caroline Ballot Sidi Mohamed Hassoun Brigitte Decoster Remi Neviere Steve Lancel
author_facet	Aurore Palud Camille Marciniak David Montaigne Xavier Marechal Caroline Ballot Sidi Mohamed Hassoun Brigitte Decoster Remi Neviere Steve Lancel
author_sort	Aurore Palud
title	Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
title_short	Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
title_full	Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
title_fullStr	Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
title_full_unstemmed	Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
title_sort	macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/f9145e85bd9e4e9fa7b5c6f95506b35f
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Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.

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