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Cell Rep. 2018 Jan 16;22(3):760-773. doi: 10.1016/j.celrep.2017.12.067.

Peroxisome Proliferator Activated Receptor Gamma Controls Mature Brown Adipocyte Inducibility through Glycerol Kinase.

Author information

1
Institute of Food, Nutrition and Health, ETH Zurich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland.
2
Functional Genomics Center Zurich, ETH Zurich/University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
3
Department of Medical and Clinical Genetics, Institute of Biomedicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg 405 30, Sweden.
4
Department of Biology, Institute for Molecular Systems Biology, Eidgenössische Technische Hochschule Zürich, 8093 Zurich, Switzerland.
5
Department of Otorhinolaryngology - Head and Neck Surgery, Faculty of Medicine and University Hospital, Comenius University, 81499 Bratislava, Slovakia.
6
Institute of Experimental Endocrinology, Biomedical Research Center at the Slovak Academy of Sciences, 84505 Bratislava, Slovakia.
7
Turku PET Centre, University of Turku, 20500 Turku, Finland; Turku University Hospital, 20500 Turku, Finland.
8
University Nice Sophia Antipolis, iBV, UMR 7277 Nice, France; CNRS, iBV UMR 7277 Nice, France; Inserm, iBV, U1091 Nice, France.
9
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232, Singapore Center for Integrative Genomics, University of Lausanne, 1015 Lausanne, Switzerland.
10
Institute of Food, Nutrition and Health, ETH Zurich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland. Electronic address: christian-wolfrum@ethz.ch.

Abstract

Peroxisome proliferator-activated receptors (PPARs) have been suggested as the master regulators of adipose tissue formation. However, their role in regulating brown fat functionality has not been resolved. To address this question, we generated mice with inducible brown fat-specific deletions of PPARα, β/δ, and γ, respectively. We found that both PPARα and β/δδ are dispensable for brown fat function. In contrast, we could show that ablation of PPARγ in vitro and in vivo led to a reduced thermogenic capacity accompanied by a loss of inducibility by β-adrenergic signaling, as well as a shift from oxidative fatty acid metabolism to glucose utilization. We identified glycerol kinase (Gyk) as a partial mediator of PPARγ function and could show that Gyk expression correlates with brown fat thermogenic capacity in human brown fat biopsies. Thus, Gyk might constitute the link between PPARγ-mediated regulation of brown fat function and activation by β-adrenergic signaling.

KEYWORDS:

PPAR alpha; PPAR gamma; brown adipose tissue; glycerol kinase; non-shivering thermogenesis

PMID:
29346772
DOI:
10.1016/j.celrep.2017.12.067
[Indexed for MEDLINE]
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