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Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1

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  • Prameladevi Chinnasamy

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Isabel Casimiro

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine)

  • Dario F. Riascos-Bernal

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Shreeganesh Venkatesh

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine)

  • Dippal Parikh

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Alishba Maira

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Aparna Srinivasan

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine)

  • Wei Zheng

    (Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Albert Einstein Cancer Center, Albert Einstein College of Medicine)

  • Elena Tarabra

    (Department of Molecular Pharmacology, Albert Einstein College of Medicine
    Department of Medicine (Endocrinology, Albert Einstein College of Medicine))

  • Haihong Zong

    (Department of Medicine (Endocrinology, Albert Einstein College of Medicine)
    Einstein-Mount Sinai Diabetes Research Center and Fleischer Institute of Diabetes and Metabolism, Albert Einstein College of Medicine)

  • Smitha Jayakumar

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine)

  • Venkatesh Jeganathan

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine)

  • Kith Pradan

    (Albert Einstein College of Medicine)

  • Jose O. Aleman

    (New York University Langone Health)

  • Rajat Singh

    (Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine
    Department of Medicine (Endocrinology, Albert Einstein College of Medicine)
    Einstein-Mount Sinai Diabetes Research Center and Fleischer Institute of Diabetes and Metabolism, Albert Einstein College of Medicine)

  • Sayan Nandi

    (Department of Developmental and Molecular Biology, Albert Einstein College of Medicine)

  • Jeffrey E. Pessin

    (Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine
    Department of Molecular Pharmacology, Albert Einstein College of Medicine
    Einstein-Mount Sinai Diabetes Research Center and Fleischer Institute of Diabetes and Metabolism, Albert Einstein College of Medicine)

  • Nicholas E. S. Sibinga

    (Department of Medicine (Cardiology), Albert Einstein College of Medicine
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine
    Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine
    Albert Einstein Cancer Center, Albert Einstein College of Medicine)

Abstract

Recent studies implicate macrophages in regulation of thermogenic, sympathetic neuron-mediated norepinephrine (NE) signaling in adipose tissues, but understanding of such non-classical macrophage activities is incomplete. Here we show that male mice lacking the allograft inflammatory factor-1 (AIF1) protein resist high fat diet (HFD)-induced obesity and hyperglycemia. We link this phenotype to higher adipose NE levels that stem from decreased monoamine oxidase A (MAOA) expression and NE clearance by AIF1-deficient macrophages, and find through reciprocal bone marrow transplantation that donor Aif1-/- vs WT genotype confers the obesity phenotype in mice. Interestingly, human sequence variants near the AIF1 locus associate with obesity and diabetes; in adipose samples from participants with obesity, we observe direct correlation of AIF1 and MAOA transcript levels. These findings identify AIF1 as a regulator of MAOA expression in macrophages and catecholamine activity in adipose tissues – limiting energy expenditure and promoting energy storage – and suggest how it might contribute to human obesity.

Suggested Citation

  • Prameladevi Chinnasamy & Isabel Casimiro & Dario F. Riascos-Bernal & Shreeganesh Venkatesh & Dippal Parikh & Alishba Maira & Aparna Srinivasan & Wei Zheng & Elena Tarabra & Haihong Zong & Smitha Jayak, 2023. "Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1," Nature Communications, Nature, vol. 14(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-022-35683-7
    DOI: 10.1038/s41467-022-35683-7
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    References listed on IDEAS

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    1. Khoa D. Nguyen & Yifu Qiu & Xiaojin Cui & Y. P. Sharon Goh & Julia Mwangi & Tovo David & Lata Mukundan & Frank Brombacher & Richard M. Locksley & Ajay Chawla, 2011. "Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis," Nature, Nature, vol. 480(7375), pages 104-108, December.
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    1. Suyang Wu & Chen Qiu & Jiahao Ni & Wenli Guo & Jiyuan Song & Xingyin Yang & Yulin Sun & Yanjun Chen & Yunxia Zhu & Xiaoai Chang & Peng Sun & Chunxia Wang & Kai Li & Xiao Han, 2024. "M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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