Boutant 2017 EMBO J: Difference between revisions
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{{Publication | {{Publication | ||
|title=Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Cantó C (2017) Mfn2 is critical for brown adipose tissue thermogenic function. EMBO J 36:1543-58. | |title=Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Cantó C (2017) Mfn2 is critical for brown adipose tissue thermogenic function. EMBO J 36:1543-58. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/28348166 PMID: 28348166] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/28348166 PMID: 28348166 Open Access] | ||
|authors=Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Canto C | |authors=Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Canto C | ||
|year=2017 | |year=2017 | ||
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|preparations=Intact cells, Homogenate, Isolated mitochondria | |preparations=Intact cells, Homogenate, Isolated mitochondria | ||
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex V;ATP synthase | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex V;ATP synthase | ||
|couplingstates=LEAK, ROUTINE, OXPHOS, | |couplingstates=LEAK, ROUTINE, OXPHOS, ET | ||
|pathways=N, S, NS, ROX | |pathways=N, S, NS, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2017-07, | |additional=2017-07, | ||
}} | }} | ||
Latest revision as of 17:00, 9 November 2017
| Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Cantó C (2017) Mfn2 is critical for brown adipose tissue thermogenic function. EMBO J 36:1543-58. |
Boutant M, Kulkarni SS, Joffraud M, Ratajczak J, Valera-Alberni M, Combe R, Zorzano A, Canto C (2017) EMBO J
Abstract: 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.
© 2017 The Authors. Published under the terms of the CC BY NC ND 4.0 license. • Keywords: Brown adipose tissue, Insulin resistance, Lipid droplet, Mitochondrial dynamics, Mitofusin 2 • Bioblast editor: Kandolf G • O2k-Network Lab: ES Barcelona Zorzano A, CH Lausanne Canto C
Labels: MiParea: Respiration, mtDNA;mt-genetics
Organism: Mouse
Tissue;cell: Fat, Fibroblast
Preparation: Intact cells, Homogenate, Isolated mitochondria
Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex V;ATP synthase
Coupling state: LEAK, ROUTINE, OXPHOS, ET Pathway: N, S, NS, ROX HRR: Oxygraph-2k
2017-07
