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Native adiponectin in serum binds to mammalian cells expressing T-cadherin, but not AdipoRs or calreticulin

  1. Shunbun Kita  Is a corresponding author
  2. Shiro Fukuda
  3. Norikazu Maeda
  4. Iichiro Shimomura
  1. Osaka University, Japan
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Cite this article as: eLife 2019;8:e48675 doi: 10.7554/eLife.48675


Adiponectin is an adipocyte-derived atypically abundant circulating factor that protects various organs and tissues through its receptors, AdipoRs, calreticulin, and T-cadherin. To identify the major binding partner of circulating native adiponectin, we expressed these receptors on the surface of HEK293 cells. Adiponectin, either that in mouse or human serum, purified from serum, or produced by mammalian cells, bound to cells expressing T-cadherin, but not to those expressing AdipoR1 or calreticulin. The stable introduction of T-cadherin and AdipoR1 into CHO cells resulted in the cell surface localization of these receptors. Native adiponectin in serum bound to cells expressing T-cadherin, not to those expressing AdipoR1. The knockdown of T-cadherin, but not AdipoRs resulted in the significant attenuation of native adiponectin binding to C2C12 myotubes. Therefore, native adiponectin binding depended on the amount of T-cadherin expressed in HEK293 cells, CHO cells, and C2C12 myotubes. Collectively, our mammalian cell-based studies suggest that T-cadherin is the major binding partner of native adiponectin in serum.

Data availability

All data were deposited in Dryad under https://dx.doi.org/10.5061/dryad.82557c0

The following data sets were generated

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Author details

  1. Shunbun Kita

    Department of Metabolic Medicine, Osaka University, Suita, Japan
    For correspondence
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-8937-0053
  2. Shiro Fukuda

    Department of Metabolic Medicine, Osaka University, Suita, Japan
    Competing interests
    The authors declare that no competing interests exist.
  3. Norikazu Maeda

    Department of Metabolic Medicine, Osaka University, Suita, Japan
    Competing interests
    The authors declare that no competing interests exist.
  4. Iichiro Shimomura

    Department of Metabolic Medicine, Osaka University, Suita, Japan
    Competing interests
    The authors declare that no competing interests exist.



  • Shiro Fukuda
  • Iichiro Shimomura


  • Shiro Fukuda
  • Iichiro Shimomura

Grant in Aid for Scientific Research (#16K09802)

  • Shunbun Kita

Grant in Aid for Scientific Research (#16K09801)

  • Norikazu Maeda

Grant in Aid for Scientific Research (#15H04853)

  • Iichiro Shimomura

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.


Animal experimentation: The experimental protocol was approved as No. 28-072-023 by the Ethics Review Committee for Animal Experimentation of Osaka University School of Medicine. This study also conformed to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health.

Reviewing Editor

  1. David E James, The University of Sydney, Australia

Publication history

  1. Received: May 22, 2019
  2. Accepted: October 13, 2019
  3. Accepted Manuscript published: October 24, 2019 (version 1)
  4. Version of Record published: October 31, 2019 (version 2)


© 2019, Kita et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.


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