Soluble LR11/SorLA represses thermogenesis in adipose tissue and correlates with BMI in humans

Andrew J. Whittle, Meizi Jiang, Vivian Peirce, Joana Relat, Sam Virtue, Hiroyuki Ebinuma, Isamu Fukamachi, Takashi Yamaguchi, Mao Takahashi, Takeyoshi Murano, Ichiro Tatsuno, Masahiro Takeuchi, Chiaki Nakaseko, Wenlong Jin, Zhehu Jin, Mark Campbell, Wolfgang J. Schneider, Antonio Vidal-Puig () and Hideaki Bujo ()
Additional contact information
Andrew J. Whittle: University of Cambridge Metabolic Research Laboratories, Level 4, Wellcome Trust-MRC Institute of Metabolic Science
Meizi Jiang: Toho University, Sakura Medical Center
Vivian Peirce: University of Cambridge Metabolic Research Laboratories, Level 4, Wellcome Trust-MRC Institute of Metabolic Science
Joana Relat: School of Pharmacy, University of Barcelona, and Institute of Biomedicine of the University of Barcelona (IBUB)
Sam Virtue: University of Cambridge Metabolic Research Laboratories, Level 4, Wellcome Trust-MRC Institute of Metabolic Science
Hiroyuki Ebinuma: Tsukuba Research Institute, Sekisui Medical Co. Ltd.
Isamu Fukamachi: Tsukuba Research Institute, Sekisui Medical Co. Ltd.
Takashi Yamaguchi: Center for Diabetes, Endocrinology and Metabolism, Toho University, Sakura Medical Center
Mao Takahashi: Cardiovascular Center, Toho University, Sakura Medical Center
Takeyoshi Murano: Toho University, Sakura Medical Center
Ichiro Tatsuno: Center for Diabetes, Endocrinology and Metabolism, Toho University, Sakura Medical Center
Masahiro Takeuchi: Chiba University Hospital
Chiaki Nakaseko: Chiba University Hospital
Wenlong Jin: Affiliated Hospital of Yanbian University
Zhehu Jin: Affiliated Hospital of Yanbian University
Mark Campbell: University of Cambridge Metabolic Research Laboratories, Level 4, Wellcome Trust-MRC Institute of Metabolic Science
Wolfgang J. Schneider: Medical University of Vienna, Max F. Perutz Laboratories
Antonio Vidal-Puig: University of Cambridge Metabolic Research Laboratories, Level 4, Wellcome Trust-MRC Institute of Metabolic Science
Hideaki Bujo: Toho University, Sakura Medical Center

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract Thermogenesis in brown adipose tissue (BAT) is an important component of energy expenditure in mammals. Recent studies have confirmed its presence and metabolic role in humans. Defining the physiological regulation of BAT is therefore of great importance for developing strategies to treat metabolic diseases. Here we show that the soluble form of the low-density lipoprotein receptor relative, LR11/SorLA (sLR11), suppresses thermogenesis in adipose tissue in a cell-autonomous manner. Mice lacking LR11 are protected from diet-induced obesity associated with an increased browning of white adipose tissue and hypermetabolism. Treatment of adipocytes with sLR11 inhibits thermogenesis via the bone morphogenetic protein/TGFβ signalling pathway and reduces Smad phosphorylation. In addition, sLR11 levels in humans are shown to positively correlate with body mass index and adiposity. Given the need for tight regulation of a tissue with a high capacity for energy wastage, we propose that LR11 plays an energy conserving role that is exaggerated in states of obesity.

Date: 2015
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DOI: 10.1038/ncomms9951

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