Abstract

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.

Highlights

  • Increasing evidence suggests that the heart controls the metabolism of peripheral organs

  • The functional significance of the interaction between the heart and peripheral tissues through natriuretic peptides remains poorly understood, these observations suggest that the heart can regulate metabolism in the adipose tissue through cardiokines

  • Eric Olson’s group reported that the heart controls systemic energy metabolism, fat mass, and body weight via microRNA-208a and Mediator complex subunit 13 (MED13) signaling (Grueter et al, 2012). miR-208a is encoded by an intron of the a-myosin heavy-chain (MHC) gene and is required for upregulation of bMHC and cardiac growth in response to pressure overload or hypothyroidism

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Summary

Introduction

Increasing evidence suggests that the heart controls the metabolism of peripheral organs. Eric Olson’s group reported that the heart controls systemic energy metabolism, fat mass, and body weight via microRNA-208a (miR-208a) and Mediator complex subunit 13 (MED13) signaling (Grueter et al, 2012). Olson and colleagues found that in mice, inhibition of miR-208a or upregulation of MED13 in the heart confers leanness and resistance to diet-induced obesity through an increase in whole-body energy consumption.

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