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An adipocyte-specific defect in oxidative phosphorylation increases systemic energy expenditure and protects against diet-induced obesity in mouse models – published online 10/01/2020

Choi figure

Min Jeong Choi, Saet-Byel Jung, Seong Eun Lee, Seul Gi Kang, Ju Hee Lee, Min Jeong Ryu, Hyo Kyun Chung, Joon Young Chang, Yong Kyung Kim, Hyun Jung Hong, Hail Kim, Hyun Jin Kim, Chul-Ho Lee, Adil Mardinoglu, Hyon-Seung Yi, Minho Shong

Adipose tissue mitochondrial oxidative phosphorylation is critical for systemic energy homeostasis, and its dysfunction has been suggested in the aetiology of insulin resistance and diabetes. To date, there is limited experimental evidence on the systemic effects of mitochondrial oxidative phosphorylation on glucose and energy homeostasis. In this issue, Choi et al (https://doi.org/10.1007/s00125-019-05082-7) report that knockout of the gene encoding mitochondrial large ribosomal subunit protein (CRIF1) paradoxically improves systemic energy homeostasis via cell-autonomous activation of the mitochondrial unfolded protein response, and via the non-cell-autonomous mitokine actions of growth differentiation factor 15 (GDF15) and fibroblast growth factor 21 (FGF21). The authors state that these findings suggest that mitokines and their receptor modulators may be potential targets for the treatment of obesity and metabolic disease.

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