PMID- 23470566
OWN - NLM
STAT- MEDLINE
DCOM- 20131210
LR  - 20190608
IS  - 1880-3873 (Electronic)
IS  - 1340-3478 (Linking)
VI  - 20
IP  - 5
DP  - 2013
TI  - Butyrate attenuates inflammation and lipolysis generated by the interaction of 
      adipocytes and macrophages.
PG  - 425-42
AB  - AIM: Paracrine interaction between macrophages and adipocytes in obese visceral 
      fat tissues is thought to be a trigger of chronic inflammation. The 
      immunomodulatory effect of the short chain fatty acid, butyric acid, has been 
      demonstrated. We hypothesize that sodium butyrate (butyrate) attenuates 
      inflammatory responses and lipolysis generated by the interaction of macrophages 
      and adipocytes. METHODS: Using contact or transwell co-culture methods with 
      differentiated 3T3-L1 adipocytes and RAW264.7 macrophages, we investigated the 
      effects of butyrate on the production of tumor necrosis factor alpha (TNF-alpha), 
      monocyte chemoattractant protein 1 (MCP-1), interleukin 6 (IL-6), and the release 
      of free glycerol, free fatty acids (FFAs) into the medium. We also examined the 
      activity of nuclear factor-kappaB (NF-kappaB) and the phosphorylation of 
      mitogen-activated protein kinases (MAPKs) in co-cultured macrophages, as well as 
      lipase activity and expression in co-cultured adipocytes. RESULTS: We found 
      increased production of TNF-alpha, MCP-1, IL-6, and free glycerol, FFAs in the 
      co-culture medium, and butyrate significantly reduced them. Butyrate inhibited 
      the phosphorylation of MAPKs, the activity of NF-kappaB in co-cultured macrophages, 
      and suppressed lipase activity in co-cultured adipocytes. Lipase inhibitors 
      significantly attenuated the production of TNF-alpha, MCP-1 and IL-6 in the 
      co-culture medium as effectively as butyrate. Butyrate suppressed the protein 
      production of adipose triglyceride lipase, hormone sensitive lipase, and fatty 
      acid-binding protein 4 in co-cultured adipocytes. Pertussis toxin, which is known 
      to block GPR41 completely, inhibited the antilipolysis effect of butyrate. 
      CONCLUSION: Butyrate suppresses inflammatory responses generated by the 
      interaction of adipocytes and macrophages through reduced lipolysis and 
      inhibition of inflammatory signaling.
FAU - Ohira, Hideo
AU  - Ohira H
AD  - Division of Clinical Nutrition, Faculty of Nutrition, Kobe Gakuin University, 
      Japan. oohira@nutr.kobegakuin.ac.jp
FAU - Fujioka, Yoshio
AU  - Fujioka Y
FAU - Katagiri, Chikae
AU  - Katagiri C
FAU - Mamoto, Rie
AU  - Mamoto R
FAU - Aoyama-Ishikawa, Michiko
AU  - Aoyama-Ishikawa M
FAU - Amako, Katsumi
AU  - Amako K
FAU - Izumi, Yoshihiro
AU  - Izumi Y
FAU - Nishiumi, Shin
AU  - Nishiumi S
FAU - Yoshida, Masaru
AU  - Yoshida M
FAU - Usami, Makoto
AU  - Usami M
FAU - Ikeda, Masamichi
AU  - Ikeda M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130307
PL  - Japan
TA  - J Atheroscler Thromb
JT  - Journal of atherosclerosis and thrombosis
JID - 9506298
RN  - 0 (Butyrates)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Fabp4 protein, mouse)
RN  - 0 (Fatty Acid-Binding Proteins)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-6)
RN  - 0 (RNA, Messenger)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - EC 3.1.1.3 (Lipase)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/*drug effects/metabolism/pathology
MH  - Animals
MH  - Butyrates/*pharmacology
MH  - Cell Line
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Coculture Techniques
MH  - Fatty Acid-Binding Proteins/biosynthesis
MH  - Fatty Acids, Nonesterified/metabolism
MH  - Inflammation/pathology/*prevention & control
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-6/biosynthesis/genetics
MH  - Lipase/antagonists & inhibitors/metabolism
MH  - Lipolysis/*drug effects
MH  - MAP Kinase Signaling System/drug effects
MH  - Macrophages/*drug effects/metabolism/pathology
MH  - Mice
MH  - Paracrine Communication/drug effects
MH  - Pertussis Toxin/pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Transcription Factor RelA/metabolism
MH  - Tumor Necrosis Factor-alpha/biosynthesis/genetics
EDAT- 2013/03/09 06:00
MHDA- 2013/12/16 06:00
CRDT- 2013/03/09 06:00
PHST- 2013/03/09 06:00 [entrez]
PHST- 2013/03/09 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - DN/JST.JSTAGE/jat/15065 [pii]
AID - 10.5551/jat.15065 [doi]
PST - ppublish
SO  - J Atheroscler Thromb. 2013;20(5):425-42. doi: 10.5551/jat.15065. Epub 2013 Mar 7.