High-fat diet and FGF21 cooperatively promote aerobic thermogenesis in mtDNA mutator mice

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Mitochondria are highly adaptable organelles that can facilitate communication between tissues to meet the energetic demands of the organism. However, the mechanisms by which mitochondria can nonautonomously relay stress signals remain poorly understood. Here we report that mitochondrial mutations in the young, preprogeroid polymerase gamma mutator (POLG) mouse produce a metabolic state of starvation. As a result, these mice exhibit signs of metabolic imbalance including thermogenic defects in brown adipose tissue (BAT). An unexpected benefit of this adaptive response is the complete resistance to diet-induced obesity when POLG mice are placed on a high-fat diet (HFD). Paradoxically, HFD further increases oxygen consumption in part by inducing thermogenesis and mitochondrial biogenesis in BAT along with enhanced expression of fibroblast growth factor 21 (FGF21). Collectively, these findings identify a mechanistic link between FGF21, a long-known marker of mitochondrial disease, and systemic metabolic adaptation in response to mitochondrial stress.
Publisher
NATL ACAD SCIENCES
Issue Date
2015-07
Language
English
Article Type
Article
Keywords

BROWN ADIPOSE-TISSUE; GROWTH-FACTOR 21; MITOCHONDRIAL DISEASE; ENERGY-EXPENDITURE; PPAR-ALPHA; POLYMERASE; ACTIVATION; EXPRESSION; PHENOTYPES; INDUCTION

Citation

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.112, no.28, pp.8714 - 8719

ISSN
0027-8424
DOI
10.1073/pnas.1509930112
URI
http://hdl.handle.net/10203/203746
Appears in Collection
MSE-Journal Papers(저널논문)
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