PMID- 16847310
OWN - NLM
STAT- MEDLINE
DCOM- 20070329
LR  - 20220227
IS  - 0022-2275 (Print)
IS  - 0022-2275 (Linking)
VI  - 47
IP  - 10
DP  - 2006 Oct
TI  - Type II nuclear hormone receptors, coactivator, and target gene repression in 
      adipose tissue in the acute-phase response.
PG  - 2179-90
AB  - The acute-phase response (APR) leads to alterations in lipid metabolism and type 
      II nuclear hormone receptors, which regulate lipid metabolism, are suppressed, in 
      liver, heart, and kidney. Here, we examine the effect of the APR in adipose 
      tissue. In mice, lipopolysaccharide produces a rapid, marked decrease in mRNA 
      levels of nuclear hormone receptors [peroxisome proliferator-activated receptor 
      gamma (PPARgamma), liver X receptor alpha (LXRalpha) and LXRbeta, thyroid 
      receptor alpha (TRalpha) and TRbeta, and retinoid X receptor alpha (RXRalpha) and 
      RXRbeta] and receptor coactivators [cAMP response element binding protein, 
      steroid receptor coactivator 1 (SRC1) and SRC2, thyroid hormone 
      receptor-associated protein, and peroxisome proliferator-activated receptor gamma 
      co-activator 1alpha (PGC1alpha) and PGC1beta] along with decreased expression of 
      target genes (adipocyte P2, phosphoenolpyruvate carboxykinase, 
      glycerol-3-phosphate acyltransferase, ABCA1, apolipoprotein E, sterol-regulatory 
      element binding protein-1c, glucose transport protein 4 (GLUT4), malic enzyme, 
      and Spot14) involved in triglyceride (TG) and carbohydrate metabolism. We show 
      that key TG synthetic enzymes, 1-acyl-sn-glycerol-3-phosphate acyltransferase-2, 
      monoacylglycerol acyltransferase 1, and diacylglycerol acyltransferase 1, are 
      PPARgamma-regulated genes and that they also decrease in the APR. In 3T3-L1 
      adipocytes, tumor necrosis factor-alpha (TNF-alpha) significantly decreases 
      PPARgamma, LXRalpha and LXRbeta, RXRalpha and RXRbeta, SRC1 and SRC2, and 
      PGC1alpha and PGC1beta mRNA levels, which are associated with a marked reduction 
      in receptor-regulated genes. Moreover, TNF-alpha significantly reduces PPAR and 
      LXR response element-driven transcription. Thus, the APR suppresses the 
      expression of many nuclear hormone receptors and their coactivators in adipose 
      tissue, which could be a mechanism to coordinately downregulate TG biosynthesis 
      and thereby redirect lipids to other critical organs during the APR.
FAU - Lu, Biao
AU  - Lu B
AD  - Metabolism Section, Department of Veterans Affairs Medical Center, University of 
      California San Francisco, San Francisco, CA 94121, USA.
FAU - Moser, Arthur H
AU  - Moser AH
FAU - Shigenaga, Judy K
AU  - Shigenaga JK
FAU - Feingold, Kenneth R
AU  - Feingold KR
FAU - Grunfeld, Carl
AU  - Grunfeld C
LA  - eng
GR  - AR-39639/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060717
PL  - United States
TA  - J Lipid Res
JT  - Journal of lipid research
JID - 0376606
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Liver X Receptors)
RN  - 0 (Nr1h3 protein, mouse)
RN  - 0 (Orphan Nuclear Receptors)
RN  - 0 (PPAR gamma)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9010-72-4 (Zymosan)
RN  - EC 2.3.- (Acyltransferases)
SB  - IM
MH  - Acute-Phase Reaction/genetics/*metabolism
MH  - Acyltransferases/metabolism
MH  - Adipocytes
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Cells, Cultured
MH  - DNA-Binding Proteins
MH  - Female
MH  - *Gene Expression Regulation
MH  - Lipopolysaccharides/metabolism
MH  - Liver X Receptors
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Orphan Nuclear Receptors
MH  - PPAR gamma
MH  - RNA, Messenger/analysis
MH  - Receptors, Cytoplasmic and Nuclear/*metabolism
MH  - Transcription, Genetic
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Zymosan/metabolism
EDAT- 2006/07/19 09:00
MHDA- 2007/03/30 09:00
CRDT- 2006/07/19 09:00
PHST- 2006/07/19 09:00 [pubmed]
PHST- 2007/03/30 09:00 [medline]
PHST- 2006/07/19 09:00 [entrez]
AID - S0022-2275(20)43405-4 [pii]
AID - 10.1194/jlr.M500540-JLR200 [doi]
PST - ppublish
SO  - J Lipid Res. 2006 Oct;47(10):2179-90. doi: 10.1194/jlr.M500540-JLR200. Epub 2006 
      Jul 17.