Attenuation of obesity-induced adipose tissue inflammation in C3H/HeJ mice carrying a Toll-like receptor 4 mutation

Takayoshi Suganami, Tae Mieda, Michiko Itoh, Yuri Shimoda, Yasutomi Kamei, Yoshihiro Ogawa

Research output: Contribution to journalArticle

151 Citations (Scopus)

Abstract

Obese adipose tissue is characterized by increased infiltration of macrophages, suggesting that they might represent an important source of inflammation. We have provided in vitro evidence that saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 (TLR4) to induce the inflammatory changes in macrophages. Here we show the attenuation of adipose tissue inflammation in C3H/HeJ mice carrying a functional mutation in the TLR4 gene relative to control C3H/HeN mice during a 16-week high-fat diet. We also find that adiponectin mRNA expression is significantly reduced by co-culture of hypertrophied 3T3-L1 adipocytes and C3H/HeN peritoneal macrophages, which is reversed, when co-cultured with C3H/HeJ peritoneal macrophages. This study provides in vivo evidence that TLR4 plays a role in obesity-related adipose tissue inflammation and thus helps to identify the therapeutic targets that may reduce obesity-induced inflammation and the metabolic syndrome.

Original languageEnglish
Pages (from-to)45-49
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume354
Issue number1
DOIs
Publication statusPublished - Mar 2 2007
Externally publishedYes

Fingerprint

Toll-Like Receptor 4
Inbred C3H Mouse
Macrophages
Adipose Tissue
Obesity
Adipocytes
Tissue
Inflammation
Mutation
Peritoneal Macrophages
Lipolysis
Adiponectin
High Fat Diet
Coculture Techniques
Nutrition
Fatty Acids
Infiltration
Ligands
Messenger RNA
Genes

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Attenuation of obesity-induced adipose tissue inflammation in C3H/HeJ mice carrying a Toll-like receptor 4 mutation. / Suganami, Takayoshi; Mieda, Tae; Itoh, Michiko; Shimoda, Yuri; Kamei, Yasutomi; Ogawa, Yoshihiro.

In: Biochemical and Biophysical Research Communications, Vol. 354, No. 1, 02.03.2007, p. 45-49.

Research output: Contribution to journalArticle

Suganami, Takayoshi ; Mieda, Tae ; Itoh, Michiko ; Shimoda, Yuri ; Kamei, Yasutomi ; Ogawa, Yoshihiro. / Attenuation of obesity-induced adipose tissue inflammation in C3H/HeJ mice carrying a Toll-like receptor 4 mutation. In: Biochemical and Biophysical Research Communications. 2007 ; Vol. 354, No. 1. pp. 45-49.
@article{48d5473341e8425ab34032c81cf0b1cc,
title = "Attenuation of obesity-induced adipose tissue inflammation in C3H/HeJ mice carrying a Toll-like receptor 4 mutation",
abstract = "Obese adipose tissue is characterized by increased infiltration of macrophages, suggesting that they might represent an important source of inflammation. We have provided in vitro evidence that saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 (TLR4) to induce the inflammatory changes in macrophages. Here we show the attenuation of adipose tissue inflammation in C3H/HeJ mice carrying a functional mutation in the TLR4 gene relative to control C3H/HeN mice during a 16-week high-fat diet. We also find that adiponectin mRNA expression is significantly reduced by co-culture of hypertrophied 3T3-L1 adipocytes and C3H/HeN peritoneal macrophages, which is reversed, when co-cultured with C3H/HeJ peritoneal macrophages. This study provides in vivo evidence that TLR4 plays a role in obesity-related adipose tissue inflammation and thus helps to identify the therapeutic targets that may reduce obesity-induced inflammation and the metabolic syndrome.",
author = "Takayoshi Suganami and Tae Mieda and Michiko Itoh and Yuri Shimoda and Yasutomi Kamei and Yoshihiro Ogawa",
year = "2007",
month = "3",
day = "2",
doi = "10.1016/j.bbrc.2006.12.190",
language = "English",
volume = "354",
pages = "45--49",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Attenuation of obesity-induced adipose tissue inflammation in C3H/HeJ mice carrying a Toll-like receptor 4 mutation

AU - Suganami, Takayoshi

AU - Mieda, Tae

AU - Itoh, Michiko

AU - Shimoda, Yuri

AU - Kamei, Yasutomi

AU - Ogawa, Yoshihiro

PY - 2007/3/2

Y1 - 2007/3/2

N2 - Obese adipose tissue is characterized by increased infiltration of macrophages, suggesting that they might represent an important source of inflammation. We have provided in vitro evidence that saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 (TLR4) to induce the inflammatory changes in macrophages. Here we show the attenuation of adipose tissue inflammation in C3H/HeJ mice carrying a functional mutation in the TLR4 gene relative to control C3H/HeN mice during a 16-week high-fat diet. We also find that adiponectin mRNA expression is significantly reduced by co-culture of hypertrophied 3T3-L1 adipocytes and C3H/HeN peritoneal macrophages, which is reversed, when co-cultured with C3H/HeJ peritoneal macrophages. This study provides in vivo evidence that TLR4 plays a role in obesity-related adipose tissue inflammation and thus helps to identify the therapeutic targets that may reduce obesity-induced inflammation and the metabolic syndrome.

AB - Obese adipose tissue is characterized by increased infiltration of macrophages, suggesting that they might represent an important source of inflammation. We have provided in vitro evidence that saturated fatty acids, which are released from hypertrophied adipocytes via the macrophage-induced adipocyte lipolysis, serve as a naturally occurring ligand for Toll-like receptor 4 (TLR4) to induce the inflammatory changes in macrophages. Here we show the attenuation of adipose tissue inflammation in C3H/HeJ mice carrying a functional mutation in the TLR4 gene relative to control C3H/HeN mice during a 16-week high-fat diet. We also find that adiponectin mRNA expression is significantly reduced by co-culture of hypertrophied 3T3-L1 adipocytes and C3H/HeN peritoneal macrophages, which is reversed, when co-cultured with C3H/HeJ peritoneal macrophages. This study provides in vivo evidence that TLR4 plays a role in obesity-related adipose tissue inflammation and thus helps to identify the therapeutic targets that may reduce obesity-induced inflammation and the metabolic syndrome.

UR - http://www.scopus.com/inward/record.url?scp=33846302361&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33846302361&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2006.12.190

DO - 10.1016/j.bbrc.2006.12.190

M3 - Article

VL - 354

SP - 45

EP - 49

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -