A-FABP mediates adaptive thermogenesis by promoting intracellular activation of thyroid hormones in brown adipocytes

Lingling Shu, Ruby L. C. Hoo (), Xiaoping Wu, Yong Pan, Ida P. C. Lee, Lai Yee Cheong, Stefan R Bornstein, Xianglu Rong, Jiao Guo and Aimin Xu ()
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Lingling Shu: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Ruby L. C. Hoo: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Xiaoping Wu: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Yong Pan: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Ida P. C. Lee: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Lai Yee Cheong: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong
Stefan R Bornstein: University of Dresden
Xianglu Rong: Joint Laboratory of Guangdong and Hong Kong on Metabolic Diseases, Guangdong Pharmaceutical University
Jiao Guo: Joint Laboratory of Guangdong and Hong Kong on Metabolic Diseases, Guangdong Pharmaceutical University
Aimin Xu: State Key Laboratory of Pharmaceutical Biotechnology, LKS Faculty of Medicine, The University of Hong Kong

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract The adipokine adipocyte fatty acid-binding protein (A-FABP) has been implicated in obesity-related cardio-metabolic complications. Here we show that A-FABP increases thermogenesis by promoting the conversion of T4 to T3 in brown adipocytes. We find that A-FABP levels are increased in both white (WAT) and brown (BAT) adipose tissues and the bloodstream in response to thermogenic stimuli. A-FABP knockout mice have reduced thermogenesis and whole-body energy expenditure after cold stress or after feeding a high-fat diet, which can be reversed by infusion of recombinant A-FABP. Mechanistically, A-FABP induces the expression of type-II iodothyronine deiodinase in BAT via inhibition of the nuclear receptor liver X receptor α, thereby leading to the conversion of thyroid hormone from its inactive form T4 to active T3. The thermogenic responses to T4 are abrogated in A-FABP KO mice, but enhanced by A-FABP. Thus, A-FABP acts as a physiological stimulator of BAT-mediated adaptive thermogenesis.

Date: 2017
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DOI: 10.1038/ncomms14147

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