期刊
EMBO MOLECULAR MEDICINE
卷 6, 期 12, 页码 1610-1621出版社
WILEY-BLACKWELL
DOI: 10.15252/emmm.201404218
关键词
energy homeostasis; mediator complex; metabolic flexibility; metabolic gene expression; metabolism
资金
- NIH [HL-077439, HL-111665, HL-093039, PO1-DK-58398, U01-HL-100401]
- Foundation Leducq Networks of Excellence
- Cancer Prevention & Research Institute of Texas
- Robert A. Welch Foundation [1-0025]
- American Heart Association [14POST18320034]
The heart requires a continuous supply of energy but has little capacity for energy storage and thus relies on exogenous metabolic sources. We previously showed that cardiac MED13 modulates systemic energy homeostasis in mice. Here, we sought to define the extra-cardiac tissue(s) that respond to cardiac MED13 signaling. We show that cardiac overexpression of MED13 in transgenic (MED13cTg) mice confers a lean phenotype that is associated with increased lipid uptake, beta-oxidation and mitochondrial content in white adipose tissue (WAT) and liver. Cardiac expression of MED13 decreases metabolic gene expression in the heart but enhances them in WAT. Although exhibiting increased energy expenditure in the fed state, MED13cTg mice metabolically adapt to fasting. Furthermore, MED13cTg hearts oxidize fuel that is readily available, rendering them more efficient in the fed state. Parabiosis experiments in which circulations of wild-type and MED13cTg mice are joined, reveal that circulating factor(s) in MED13cTg mice promote enhanced metabolism and leanness. These findings demonstrate that MED13 acts within the heart to promote systemic energy expenditure in extra-cardiac energy depots and point to an unexplored metabolic communication system between the heart and other tissues.
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