Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor: TNFα enhances GPR84 expression in adipocytes

Hiroshi Nagasaki; Takaaki Kondo; Masahiro Fuchigami; Hiroyuki Hashimoto; Yoshihisa Sugimura; Nobuaki Ozaki; Hiroshi Arima; Akira Ota; Yutaka Oiso; Yoji Hamada

doi:10.1016/j.febslet.2012.01.001

Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor: TNFα enhances GPR84 expression in adipocytes

Hiroshi Nagasaki, Takaaki Kondo, Masahiro Fuchigami, Hiroyuki Hashimoto, Yoshihisa Sugimura, Nobuaki Ozaki, Hiroshi Arima, Akira Ota, Yutaka Oiso, Yoji Hamada

生理学Ⅰ

研究成果: Article › 査読

47 被引用数 (Scopus)

抄録

In this study we aimed to identify the physiological roles of G protein-coupled receptor 84 (GPR84) in adipose tissue, together with medium-chain fatty acids (MCFAs), the specific ligands for GPR84. In mice, high-fat diet up-regulated GPR84 expression in fat pads. In 3T3-L1 adipocytes, co-culture with a macrophage cell line, RAW264, or TNFα remarkably enhanced GPR84 expression. In the presence of TNFα, MCFAs down-regulated adiponectin mRNA expression in 3T3-L1 adipocytes. Taken together, our results suggest that GPR84 emerges in adipocytes in response to TNFα from infiltrating macrophages and exacerbates the vicious cycle between adiposity and diabesity.

本文言語	English
ページ（範囲）	368-372
ページ数	5
ジャーナル	FEBS Letters
巻	586
号	4
DOI	https://doi.org/10.1016/j.febslet.2012.01.001
出版ステータス	Published - 17-02-2012

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

文献へのアクセス

10.1016/j.febslet.2012.01.001

フィンガープリント「Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor: TNFα enhances GPR84 expression in adipocytes」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル

Nagasaki, Hiroshi ; Kondo, Takaaki ; Fuchigami, Masahiro ; Hashimoto, Hiroyuki ; Sugimura, Yoshihisa ; Ozaki, Nobuaki ; Arima, Hiroshi ; Ota, Akira ; Oiso, Yutaka ; Hamada, Yoji. / Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor : TNFα enhances GPR84 expression in adipocytes. In: FEBS Letters. 2012 ; Vol. 586, No. 4. pp. 368-372.

@article{c8c2aaa0e42d4a6aa46322afa47a25c8,

title = "Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor: TNFα enhances GPR84 expression in adipocytes",

abstract = "In this study we aimed to identify the physiological roles of G protein-coupled receptor 84 (GPR84) in adipose tissue, together with medium-chain fatty acids (MCFAs), the specific ligands for GPR84. In mice, high-fat diet up-regulated GPR84 expression in fat pads. In 3T3-L1 adipocytes, co-culture with a macrophage cell line, RAW264, or TNFα remarkably enhanced GPR84 expression. In the presence of TNFα, MCFAs down-regulated adiponectin mRNA expression in 3T3-L1 adipocytes. Taken together, our results suggest that GPR84 emerges in adipocytes in response to TNFα from infiltrating macrophages and exacerbates the vicious cycle between adiposity and diabesity.",

author = "Hiroshi Nagasaki and Takaaki Kondo and Masahiro Fuchigami and Hiroyuki Hashimoto and Yoshihisa Sugimura and Nobuaki Ozaki and Hiroshi Arima and Akira Ota and Yutaka Oiso and Yoji Hamada",

year = "2012",

month = feb,

day = "17",

doi = "10.1016/j.febslet.2012.01.001",

language = "English",

volume = "586",

pages = "368--372",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "4",

}

Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor : TNFα enhances GPR84 expression in adipocytes. / Nagasaki, Hiroshi; Kondo, Takaaki; Fuchigami, Masahiro; Hashimoto, Hiroyuki; Sugimura, Yoshihisa; Ozaki, Nobuaki; Arima, Hiroshi; Ota, Akira; Oiso, Yutaka; Hamada, Yoji.

In: FEBS Letters, Vol. 586, No. 4, 17.02.2012, p. 368-372.

研究成果: Article › 査読

TY - JOUR

T1 - Inflammatory changes in adipose tissue enhance expression of GPR84, a medium-chain fatty acid receptor

T2 - TNFα enhances GPR84 expression in adipocytes

AU - Nagasaki, Hiroshi

AU - Kondo, Takaaki

AU - Fuchigami, Masahiro

AU - Hashimoto, Hiroyuki

AU - Sugimura, Yoshihisa

AU - Ozaki, Nobuaki

AU - Arima, Hiroshi

AU - Ota, Akira

AU - Oiso, Yutaka

AU - Hamada, Yoji

PY - 2012/2/17

Y1 - 2012/2/17

N2 - In this study we aimed to identify the physiological roles of G protein-coupled receptor 84 (GPR84) in adipose tissue, together with medium-chain fatty acids (MCFAs), the specific ligands for GPR84. In mice, high-fat diet up-regulated GPR84 expression in fat pads. In 3T3-L1 adipocytes, co-culture with a macrophage cell line, RAW264, or TNFα remarkably enhanced GPR84 expression. In the presence of TNFα, MCFAs down-regulated adiponectin mRNA expression in 3T3-L1 adipocytes. Taken together, our results suggest that GPR84 emerges in adipocytes in response to TNFα from infiltrating macrophages and exacerbates the vicious cycle between adiposity and diabesity.

AB - In this study we aimed to identify the physiological roles of G protein-coupled receptor 84 (GPR84) in adipose tissue, together with medium-chain fatty acids (MCFAs), the specific ligands for GPR84. In mice, high-fat diet up-regulated GPR84 expression in fat pads. In 3T3-L1 adipocytes, co-culture with a macrophage cell line, RAW264, or TNFα remarkably enhanced GPR84 expression. In the presence of TNFα, MCFAs down-regulated adiponectin mRNA expression in 3T3-L1 adipocytes. Taken together, our results suggest that GPR84 emerges in adipocytes in response to TNFα from infiltrating macrophages and exacerbates the vicious cycle between adiposity and diabesity.

UR - http://www.scopus.com/inward/record.url?scp=84857051975&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84857051975&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2012.01.001

DO - 10.1016/j.febslet.2012.01.001

M3 - Article

C2 - 22245676

AN - SCOPUS:84857051975

VL - 586

SP - 368

EP - 372

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 4

ER -