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Heart over mind: metabolic control of white adipose tissue and liver

Increasing evidence suggests that the heart controls the metabolism of peripheral organs. Olson and colleagues previously demonstrated that miR-208a controls systemic energy homeostasis through the regulation of MED13 in cardiomyocytes (Grueter et al, 2012). In their follow-up study in this issue of...

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Detalles Bibliográficos
Autores principales: Nakamura, Michinari, Sadoshima, Junichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287972/
https://www.ncbi.nlm.nih.gov/pubmed/25471454
http://dx.doi.org/10.15252/emmm.201404749
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author Nakamura, Michinari
Sadoshima, Junichi
author_facet Nakamura, Michinari
Sadoshima, Junichi
author_sort Nakamura, Michinari
collection PubMed
description Increasing evidence suggests that the heart controls the metabolism of peripheral organs. Olson and colleagues previously demonstrated that miR-208a controls systemic energy homeostasis through the regulation of MED13 in cardiomyocytes (Grueter et al, 2012). In their follow-up study in this issue of EMBO Molecular Medicine, white adipose tissue (WAT) and liver are identified as the physiological targets of cardiac MED13 signaling, most likely through cardiac-derived circulating factors, which boost energy consumption by upregulating metabolic gene expression and increasing mitochondrial numbers (Baskin et al, 2014). In turn, increased energy expenditure in WAT and the liver confers leanness. These findings strengthen the evidence of metabolic crosstalk between the heart and peripheral tissues through cardiokines and also set the stage for the development of novel treatments for metabolic syndrome.
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spelling pubmed-42879722015-01-12 Heart over mind: metabolic control of white adipose tissue and liver Nakamura, Michinari Sadoshima, Junichi EMBO Mol Med Closeups Increasing evidence suggests that the heart controls the metabolism of peripheral organs. Olson and colleagues previously demonstrated that miR-208a controls systemic energy homeostasis through the regulation of MED13 in cardiomyocytes (Grueter et al, 2012). In their follow-up study in this issue of EMBO Molecular Medicine, white adipose tissue (WAT) and liver are identified as the physiological targets of cardiac MED13 signaling, most likely through cardiac-derived circulating factors, which boost energy consumption by upregulating metabolic gene expression and increasing mitochondrial numbers (Baskin et al, 2014). In turn, increased energy expenditure in WAT and the liver confers leanness. These findings strengthen the evidence of metabolic crosstalk between the heart and peripheral tissues through cardiokines and also set the stage for the development of novel treatments for metabolic syndrome. BlackWell Publishing Ltd 2014-12 2014-12-03 /pmc/articles/PMC4287972/ /pubmed/25471454 http://dx.doi.org/10.15252/emmm.201404749 Text en © 2014 The Authors. Published under the terms of the CC BY 4.0 license http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Closeups
Nakamura, Michinari
Sadoshima, Junichi
Heart over mind: metabolic control of white adipose tissue and liver
title Heart over mind: metabolic control of white adipose tissue and liver
title_full Heart over mind: metabolic control of white adipose tissue and liver
title_fullStr Heart over mind: metabolic control of white adipose tissue and liver
title_full_unstemmed Heart over mind: metabolic control of white adipose tissue and liver
title_short Heart over mind: metabolic control of white adipose tissue and liver
title_sort heart over mind: metabolic control of white adipose tissue and liver
topic Closeups
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4287972/
https://www.ncbi.nlm.nih.gov/pubmed/25471454
http://dx.doi.org/10.15252/emmm.201404749
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