期刊
EMBO JOURNAL
卷 36, 期 11, 页码 1543-1558出版社
WILEY
DOI: 10.15252/embj.201694914
关键词
brown adipose tissue; insulin resistance; lipid droplet; mitochondrial dynamics; mitofusin 2
资金
- MINECO [SAF2013-40987R]
- Generalitat de Catalunya [2014SGR48]
- CIBERDEM (Instituto de Salud Carlos III)
- Instituto de Salud Carlos III [PIE14/00045]
- ICREA Academia (Generalitat de Catalunya)
- EU Marie Sklodowska-Curie ITN-ChroMe (H2020-MSCA-ITN-ChroMe) [675610]
- Marie Curie Actions (MSCA) [675610] Funding Source: Marie Curie Actions (MSCA)
Mitochondrial fusion and fission events, collectively known as mitochondrial dynamics, act as quality control mechanisms to ensure mitochondrial function and fine-tune cellular bioenergetics. Defective mitofusin 2 (Mfn2) expression and enhanced mitochondrial fission in skeletal muscle are hallmarks of insulin-resistant states. Interestingly, Mfn2 is highly expressed in brown adipose tissue (BAT), yet its role remains unexplored. Using adipose-specific Mfn2 knockout (Mfn2-adKO) mice, we demonstrate that Mfn2, but not Mfn1, deficiency in BAT leads to a profound BAT dysfunction, associated with impaired respiratory capacity and a blunted response to adrenergic stimuli. Importantly, Mfn2 directly interacts with perilipin 1, facilitating the interaction between the mitochondria and the lipid droplet in response to adrenergic stimulation. Surprisingly, Mfn2-adKO mice were protected from high-fat diet-induced insulin resistance and hepatic steatosis. Altogether, these results demonstrate that Mfn2 is a mediator of mitochondria to lipid droplet interactions, influencing lipolytic processes and whole-body energy homeostasis.
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