PMID- 22033411
OWN - NLM
STAT- MEDLINE
DCOM- 20120112
LR  - 20111114
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 415
IP  - 1
DP  - 2011 Nov 11
TI  - Suppression of lipin-1 expression increases monocyte chemoattractant protein-1 
      expression in 3T3-L1 adipocytes.
PG  - 200-5
LID - 10.1016/j.bbrc.2011.10.060 [doi]
AB  - Lipin-1 plays a crucial role in the regulation of lipid metabolism and cell 
      differentiation in adipocytes. Expression of adipose lipin-1 is reduced in 
      obesity, and metabolic syndrome. However, the significance of this reduction 
      remains unclear. This study investigated if and how reduced lipin-1 expression 
      affected metabolism. We assessed mRNA expression levels of various genes related 
      to adipocyte metabolism in lipin-1-depleted 3T3-L1 adipocytes by introducing its 
      specific small interfering RNA. In lipin-1-depleted adipocytes, mRNA and protein 
      expression levels of monocyte chemoattractant protein-1 (MCP-1) were 
      significantly increased, although the other genes tested were not altered. The 
      conditioned media from the cells promoted monocyte chemotaxis. The increase in 
      MCP-1 expression was prevented by treatment with quinazoline or salicylate, 
      inhibitors of nuclear factor-kappaB activation. Because MCP-1 is related to adipose 
      inflammation and systemic insulin resistance, these results suggest that a 
      reduction in adipose lipin-1 in obesity may exacerbate adipose inflammation and 
      metabolism.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Takahashi, Nobuhiko
AU  - Takahashi N
AD  - Department of Internal Medicine, School of Dentistry, Health Sciences University 
      of Hokkaido, 1757 Kanazawa, Ishikari-Toubetsu, Hokkaido 061-0023, Japan. 
      ntkhs@hoku-iryo-u.ac.jp
FAU - Yoshizaki, Takayuki
AU  - Yoshizaki T
FAU - Hiranaka, Natsumi
AU  - Hiranaka N
FAU - Suzuki, Takeshi
AU  - Suzuki T
FAU - Yui, Tomoo
AU  - Yui T
FAU - Akanuma, Masayasu
AU  - Akanuma M
FAU - Oka, Kazuya
AU  - Oka K
FAU - Kanazawa, Kaoru
AU  - Kanazawa K
FAU - Yoshida, Mika
AU  - Yoshida M
FAU - Naito, Sumiyoshi
AU  - Naito S
FAU - Fujiya, Mikihiro
AU  - Fujiya M
FAU - Kohgo, Yutaka
AU  - Kohgo Y
FAU - Ieko, Masahiro
AU  - Ieko M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111018
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Quinazolines)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Salicylates)
RN  - EC 3.1.3.4 (Lpin1 protein, mouse)
RN  - EC 3.1.3.4 (Phosphatidate Phosphatase)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/*metabolism
MH  - Animals
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemotaxis
MH  - Gene Expression
MH  - Insulin Resistance
MH  - Mice
MH  - NF-kappa B/antagonists & inhibitors/metabolism
MH  - Nuclear Proteins/antagonists & inhibitors/genetics/*metabolism
MH  - Obesity/genetics/*metabolism
MH  - Phosphatidate Phosphatase/antagonists & inhibitors/genetics/*metabolism
MH  - Protein Biosynthesis
MH  - Quinazolines/pharmacology
MH  - RNA, Messenger/biosynthesis
MH  - RNA, Small Interfering/genetics
MH  - Salicylates/pharmacology
EDAT- 2011/10/29 06:00
MHDA- 2012/01/13 06:00
CRDT- 2011/10/29 06:00
PHST- 2011/10/10 00:00 [received]
PHST- 2011/10/11 00:00 [accepted]
PHST- 2011/10/29 06:00 [entrez]
PHST- 2011/10/29 06:00 [pubmed]
PHST- 2012/01/13 06:00 [medline]
AID - S0006-291X(11)01857-2 [pii]
AID - 10.1016/j.bbrc.2011.10.060 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2011 Nov 11;415(1):200-5. doi: 
      10.1016/j.bbrc.2011.10.060. Epub 2011 Oct 18.