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Cited 37 time in webofscience Cited 40 time in scopus
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Mitohormesis in Hypothalamic POMC Neurons Mediates Regular Exercise-Induced High-Turnover Metabolism

Authors
Kang, G.M.Min, S.H.Lee, C.H.Kim, J.Y.Lim, H.S.Choi, M.J.Jung, S.-B.Park, J.W.Kim, S.Park, C.B.Dugu, H.Choi, J.H.Jang, W.H.Park, S.E.Cho, Y.M.Kim, J.G.Kim, K.-G.Choi, C.S.Kim, Y.-B.Lee, C.Shong, M.Kim, M.-S.
Issue Date
2-Feb-2021
Publisher
Cell Press
Keywords
adipose; exercise; hypothalamus; metabolism; mitochondria; obesity; proopiomelanocortin; ribosome; stress; thermogenesis
Citation
Cell Metabolism, v.33, no.2, pp.334 - 349.e6
Journal Title
Cell Metabolism
Volume
33
Number
2
Start Page
334
End Page
349.e6
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/80832
DOI
10.1016/j.cmet.2021.01.003
ISSN
1550-4131
Abstract
Low-grade mitochondrial stress can promote health and longevity, a phenomenon termed mitohormesis. Here, we demonstrate the opposing metabolic effects of low-level and high-level mitochondrial ribosomal (mitoribosomal) stress in hypothalamic proopiomelanocortin (POMC) neurons. POMC neuron-specific severe mitoribosomal stress due to Crif1 homodeficiency causes obesity in mice. By contrast, mild mitoribosomal stress caused by Crif1 heterodeficiency in POMC neurons leads to high-turnover metabolism and resistance to obesity. These metabolic benefits are mediated by enhanced thermogenesis and mitochondrial unfolded protein responses (UPRmt) in distal adipose tissues. In POMC neurons, partial Crif1 deficiency increases the expression of β-endorphin (β-END) and mitochondrial DNA-encoded peptide MOTS-c. Central administration of MOTS-c or β-END recapitulates the adipose phenotype of Crif1 heterodeficient mice, suggesting these factors as potential mediators. Consistently, regular running exercise at moderate intensity stimulates hypothalamic MOTS-c/β-END expression and induces adipose tissue UPRmt and thermogenesis. Our findings indicate that POMC neuronal mitohormesis may underlie exercise-induced high-turnover metabolism. Kang et al. demonstrate that high-level mitochondrial stress in POMC-producing neurons causes severe obesity. In contrast, low-level mitochondrial stress in the same neurons enhances thermogenesis in the adipose tissue and protects against obesity via interorgan mitochondrial stress responses between the brain and adipose tissue. © 2021 Elsevier Inc.
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