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Title: Activin E Controls Energy Homeostasis in Both Brown and White Adipose Tissues as a Hepatokine
Authors: Hashimoto, Osamu
Funaba, Masayuki  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-4303-6682 (unconfirmed)
Sekiyama, Kazunari
Doi, Satoru
Shindo, Daichi
Satoh, Ryo
Itoi, Hiroshi
Oiwa, Hiroaki
Morita, Masahiro
Suzuki, Chisato
Sugiyama, Makoto
Yamakawa, Norio
Takada, Hitomi
Matsumura, Shigenobu  kyouindb  KAKEN_id
Inoue, Kazuo  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0001-7003-8635 (unconfirmed)
Oyadomari, Seiichi
Sugino, Hiromu
Kurisaki, Akira
Author's alias: 橋本, 統
舟場, 正幸
関山, 一成
杉山, 真言
高田, 仁実
松村, 成暢
井上, 和生
親泊, 政一
杉野, 弘
栗崎, 晃
Keywords: activin E
beige adipocyte
brown adipocyte
browning
hepatokine
Inhbe
insulin sensitivity
nonshivering thermogenesis
obesity
Issue Date: 30-Oct-2018
Publisher: Elsevier BV
Journal title: Cell Reports
Volume: 25
Issue: 5
Start page: 1193
End page: 1203
Abstract: Brown adipocyte activation or beige adipocyte emergence in white adipose tissue (WAT) increases energy expenditure, leading to a reduction in body fat mass and improved glucose metabolism. We found that activin E functions as a hepatokine that enhances thermogenesis in response to cold exposure through beige adipocyte emergence in inguinal WAT (ingWAT). Hepatic activin E overexpression activated thermogenesis through Ucp1 upregulation in ingWAT and other adipose tissues including interscapular brown adipose tissue and mesenteric WAT. Hepatic activin E-transgenic mice exhibited improved insulin sensitivity. Inhibin βE gene silencing inhibited cold-induced Ucp1 induction in ingWAT. Furthermore, in vitro experiments suggested that activin E directly stimulated expression of Ucp1 and Fgf21, which was mediated by transforming growth factor-β or activin type I receptors. We uncovered a function of activin E to stimulate energy expenditure through brown and beige adipocyte activation, suggesting a possible preventive or therapeutic target for obesity.
Description: アクチビンEが脂肪燃焼細胞の増加を促進することを解明 --肥満解消の新たなプレイヤーを発見--. 京都大学プレスリリース. 2018-11-02.
Rights: © 2018 The Authors. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
URI: http://hdl.handle.net/2433/234944
DOI(Published Version): 10.1016/j.celrep.2018.10.008
PubMed ID: 30380411
Related Link: http://www.kyoto-u.ac.jp/ja/research/research_results/2018/181031_1.html
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