Review Series 10.1172/JCI129193
1Department of Metabolic Medicine,
2Department of Adipose Management, and
3Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, Osaka, Japan.
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@endmet.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@endmet.med.osaka-u.ac.jp.
Find articles by
Kita, S.
in:
JCI
|
PubMed
|
Google Scholar
|
1Department of Metabolic Medicine,
2Department of Adipose Management, and
3Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, Osaka, Japan.
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@endmet.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@endmet.med.osaka-u.ac.jp.
Find articles by Maeda, N. in: JCI | PubMed | Google Scholar
1Department of Metabolic Medicine,
2Department of Adipose Management, and
3Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, Osaka, Japan.
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@endmet.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@endmet.med.osaka-u.ac.jp.
Find articles by Shimomura, I. in: JCI | PubMed | Google Scholar
First published September 4, 2019 - More info
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.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.