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Fibroblast growth factor 21 increases insulin sensitivity through specific expansion of subcutaneous fat

Author

Listed:
  • Huating Li

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital
    State Key Laboratory of Pharmaceutical Biotechnology
    The University of Hong Kong)

  • Guangyu Wu

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital
    Shanghai Jiao Tong University School of Medicine)

  • Qichen Fang

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital)

  • Mingliang Zhang

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital)

  • Xiaoyan Hui

    (State Key Laboratory of Pharmaceutical Biotechnology
    The University of Hong Kong)

  • Bin Sheng

    (Shanghai Jiao Tong University)

  • Liang Wu

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital
    Shanghai Jiao Tong University School of Medicine)

  • Yuqian Bao

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital)

  • Peng Li

    (Tsinghua University)

  • Aimin Xu

    (State Key Laboratory of Pharmaceutical Biotechnology
    The University of Hong Kong)

  • Weiping Jia

    (Shanghai Jiao Tong University Affiliated Sixth People’s Hospital)

Abstract

Although the pharmacological effects of fibroblast growth factor 21 (FGF21) are well-documented, uncertainty about its role in regulating excessive energy intake remains. Here, we show that FGF21 improves systemic insulin sensitivity by promoting the healthy expansion of subcutaneous adipose tissue (SAT). Serum FGF21 levels positively correlate with the SAT area in insulin-sensitive obese individuals. FGF21 knockout mice (FGF21KO) show less SAT mass and are more insulin-resistant when fed a high-fat diet. Replenishment of recombinant FGF21 to a level equivalent to that in obesity restores SAT mass and reverses insulin resistance in FGF21KO, but not in adipose-specific βklotho knockout mice. Moreover, transplantation of SAT from wild-type to FGF21KO mice improves insulin sensitivity in the recipients. Mechanistically, circulating FGF21 upregulates adiponectin in SAT, accompanied by an increase of M2 macrophage polarization. We propose that elevated levels of endogenous FGF21 in obesity serve as a defense mechanism to protect against systemic insulin resistance.

Suggested Citation

  • Huating Li & Guangyu Wu & Qichen Fang & Mingliang Zhang & Xiaoyan Hui & Bin Sheng & Liang Wu & Yuqian Bao & Peng Li & Aimin Xu & Weiping Jia, 2018. "Fibroblast growth factor 21 increases insulin sensitivity through specific expansion of subcutaneous fat," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02677-9
    DOI: 10.1038/s41467-017-02677-9
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    Cited by:

    1. Kang Chen & Lai Yee Cheong & Yuan Gao & Yaming Zhang & Tianshi Feng & Qin Wang & Leigang Jin & Eric Honoré & Karen S. L. Lam & Weiping Wang & Xiaoyan Hui & Aimin Xu, 2022. "Adipose-targeted triiodothyronine therapy counteracts obesity-related metabolic complications and atherosclerosis with negligible side effects," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    2. Shaojian Lin & Anke Zhang & Ling Yuan & Yufan Wang & Chuan Zhang & Junkun Jiang & Houshi Xu & Huiwen Yuan & Hui Yao & Qianying Zhang & Yong Zhang & Meiqing Lou & Ping Wang & Zhen-Ning Zhang & Bing Lua, 2022. "Targeting parvalbumin promotes M2 macrophage polarization and energy expenditure in mice," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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