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      Interorgan communication by exosomes, adipose tissue, and adiponectin in metabolic syndrome

      review-article
      1 , 2 , , 1 , 3 , 1
      The Journal of Clinical Investigation
      American Society for Clinical Investigation

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          Abstract

          Adipose tissue plays important roles in regulating whole-body energy metabolism through its storage function in white adipocytes and its dissipating function in brown and beige adipocytes. Adipose tissue also produces a variety of secreted factors called adipocytokines, including leptin and adiponectin. Furthermore, recent studies have suggested the important roles of extracellular vesicles of endosomal origin termed exosomes, which are secreted from adipocytes and other cells in adipose tissue and influence whole-body glucose and lipid metabolism. Adiponectin is known to be a pleiotropic organ-protective protein that is exclusively produced by adipocytes and decreased in obesity. Adiponectin accumulates in tissues such as heart, muscle, and vascular endothelium through binding with T-cadherin, a glycosylphosphatidylinositol-anchored (GPI-anchored) cadherin. Recently, adiponectin was found to enhance exosome biogenesis and secretion, leading to a decrease in cellular ceramides, excess of which is known to cause insulin resistance and cardiovascular disease phenotypes. These findings support the hypothesis that adipose tissue metabolism systemically regulates exosome production and whole-body metabolism through exosomes. This review focuses on intra-adipose and interorgan communication by exosomes, adiponectin-stimulated exosome production, and their dysregulation in metabolic diseases.

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          Author and article information

          Contributors
          Journal
          J Clin Invest
          J. Clin. Invest
          J Clin Invest
          The Journal of Clinical Investigation
          American Society for Clinical Investigation
          0021-9738
          1558-8238
          4 September 2019
          4 September 2019
          1 October 2019
          1 October 2020
          : 129
          : 10
          : 4041-4049
          Affiliations
          [1 ]Department of Metabolic Medicine,
          [2 ]Department of Adipose Management, and
          [3 ]Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, Osaka, Japan.
          Author notes
          Address correspondence to: Shunbun Kita, Department of Metabolic Medicine and Department of Adipose Tissue Management, Graduate School of Medicine, Osaka University, 2-2 Suita, Osaka 565-0871, Japan. Phone: 81.6.6879.3737; Email: shunkita@ 123456endmet.med.osaka-u.ac.jp . Or to: Iichiro Shimomura, Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2 Suita, Osaka 565-0871, Japan. Phone: 81.6.6879.3744; Email: ichi@ 123456endmet.med.osaka-u.ac.jp .
          Author information
          http://orcid.org/0000-0002-8937-0053
          Article
          PMC6763291 PMC6763291 6763291 129193
          10.1172/JCI129193
          6763291
          31483293
          bcdef2ae-8282-4322-9907-8b13aa1b0450
          © 2019 American Society for Clinical Investigation
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