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

Journal article
Authors D. Lasar
M. Rosenwald
E. Kiehlmann
M. Balaz
B. Tall
L. Opitz
Martin Lidell
N. Zamboni
P. Krznar
W. F. Sun
L. Varga
P. Stefanicka
J. Ukropec
P. Nuutila
K. Virtanen
E. Z. Amri
Sven Enerbäck
W. Wahli
C. Wolfrum
Published in Cell Reports
Volume 22
Issue 3
Pages 760-773
ISSN 2211-1247
Publication year 2018
Published at Institute of Biomedicine, Department of Medical and Clinical Genetics
Pages 760-773
Language en
Keywords uncoupling protein-1 gene, ppar-gamma, adipose-tissue, insulin-resistance, white adipocytes, energy-metabolism, fat, expression, obesity, alpha, Cell Biology, akrabarty k, 1983, journal of lipid research, v24, p381
Subject categories Genetics


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 PPAR alpha, beta/delta, and gamma, respectively. We found that both PPARa and beta/delta are dispensable for brown fat function. In contrast, we could show that ablation of PPAR gamma in vitro and in vivo led to a reduced thermogenic capacity accompanied by a loss of inducibility by beta-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 PPAR gamma 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 PPAR gamma-mediated regulation of brown fat function and activation by b-adrenergic signaling.

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