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Cell Rep. 2019 Mar 12;26(11):2849-2858.e4. doi: 10.1016/j.celrep.2019.02.039.

Mitofusin 2 in Mature Adipocytes Controls Adiposity and Body Weight.

Author information

1
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: giacomo.mancini@yale.edu.
2
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
3
Medical Department, University of Leipzig, 04103 Leipzig, Germany.
4
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Anatomy and Histology, University of Veterinary Medicine, Budapest 1078, Hungary. Electronic address: tamas.horvath@yale.edu.

Abstract

We found that exposure of adult animals to calorie-dense foods rapidly abolished expression of mitofusin 2 (Mfn2), a gene promoting mitochondrial fusion and mitochondrion-endoplasmic reticulum interactions, in white and brown fat. Mfn2 mRN was also robustly lower in obese human subjects compared with lean controls. Adipocyte-specific knockdown of Mfn2 in adult mice led to increased food intake, adiposity, and impaired glucose metabolism on standard chow as well as on a diet with high calorie content. The body weight and adiposity of mature adipocyte-specific Mfn2 knockout mice on a standard diet were similar to those of control mice on a high-fat diet. The transcriptional profile of the adipose tissue in adipocyte-specific Mfn2 knockout mice was consistent with adipocyte proliferation, increased lipogenesis at the tissue level, and decreased glucose utilization at the systemic level. These observations suggest a possible crucial role for mitochondrial dynamics in adipocytes in initiating systemic metabolic dysregulation.

KEYWORDS:

mitochondria; mitofusin; obesity; white adipocyte

PMID:
30865877
DOI:
10.1016/j.celrep.2019.02.039
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