PMID- 18492809
OWN - NLM
STAT- MEDLINE
DCOM- 20090710
LR  - 20181201
IS  - 1479-6805 (Electronic)
IS  - 0022-0795 (Linking)
VI  - 198
IP  - 2
DP  - 2008 Aug
TI  - Cyclooxygenase-2 [corrected] activation by endotoxin mediates the decrease in 
      IGF1, but not in IGFBP3, [corrected] gene expression in the liver.
PG  - 385-94
LID - 10.1677/JOE-08-0205 [doi]
AB  - The aim of this work was to analyse the role of cyclooxygenase-2 (Ptgs2) in 
      endotoxin-induced decrease in Igf1 and Igf binding protein-3 (Igfbp3). For this 
      purpose, male Wistar rats were injected with lipolysaccharide (LPS) and/or the 
      Ptgs2 inhibitor meloxicam. LPS induced a significant decrease (P<0.01) in serum 
      concentrations of Igf1 and Igfbp3 and their mRNAs in the liver. Meloxicam 
      administration prevented the inhibitory effect of LPS injection on serum Igf1 and 
      its liver mRNA. By contrast, meloxicam administration was unable to modify the 
      inhibitory effect of LPS on Igfbp3. LPS injection also induced a decrease in GH 
      receptor (Ghr) mRNA in the liver, and meloxicam attenuated this effect. In order 
      to elucidate a direct action of the Ptgs2 inhibitor on the liver cells, the 
      effect of LPS and/or meloxicam was studied in primary cultures of hepatocytes 
      with non-parenchymal cells. LPS decreased Igf1 and Ghr but not Igfbp3 gene 
      expression in liver cells in culture. Meloxicam administration attenuated the 
      inhibitory effect of LPS on Igf1 mRNA, whereas it did not modify the decrease in 
      Ghr mRNA after LPS. The effect of meloxicam on the LPS response does not seem to 
      be mediated by changes in nitric oxide or tumour necrosis factor (Tnf) 
      production, since meloxicam did not modify the stimulatory effect of LPS on 
      nitric oxide or Tnfalpha gene expression both in vivo and in vitro. All these 
      data suggest that LPS-induced Ptgs2 activation decreases Igf1 gene expression in 
      liver cells.
FAU - Martin, A I
AU  - Martin AI
AD  - Department of Physiology, Faculty of Medicine, University Complutense of Madrid, 
      28040 Madrid, Spain.
FAU - Lopez-Menduina, M
AU  - Lopez-Menduina M
FAU - Castillero, E
AU  - Castillero E
FAU - Granado, M
AU  - Granado M
FAU - Villanua, M A
AU  - Villanua MA
FAU - Lopez-Calderon, A
AU  - Lopez-Calderon A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080520
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Insulin-Like Growth Factor Binding Protein 3)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nitrates)
RN  - 0 (Nitrites)
RN  - 0 (Thiazines)
RN  - 0 (Thiazoles)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (Ptgs2 protein, rat)
RN  - VG2QF83CGL (Meloxicam)
SB  - IM
EIN - J Endocrinol. 2008 Dec;199(3):501
MH  - Animals
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Cyclooxygenase 2/*metabolism
MH  - Cyclooxygenase Inhibitors/pharmacology
MH  - Enzyme Activation/drug effects
MH  - Insulin-Like Growth Factor Binding Protein 3/genetics/*metabolism
MH  - Insulin-Like Growth Factor I/genetics/*metabolism
MH  - Lipopolysaccharides/*pharmacology
MH  - Liver/*drug effects/*metabolism
MH  - Male
MH  - Meloxicam
MH  - Nitrates/metabolism
MH  - Nitrites/metabolism
MH  - Polymerase Chain Reaction
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Thiazines/pharmacology
MH  - Thiazoles/pharmacology
MH  - Tumor Necrosis Factor-alpha/genetics
EDAT- 2008/05/22 09:00
MHDA- 2009/07/11 09:00
CRDT- 2008/05/22 09:00
PHST- 2008/05/22 09:00 [pubmed]
PHST- 2009/07/11 09:00 [medline]
PHST- 2008/05/22 09:00 [entrez]
AID - JOE-08-0205 [pii]
AID - 10.1677/JOE-08-0205 [doi]
PST - ppublish
SO  - J Endocrinol. 2008 Aug;198(2):385-94. doi: 10.1677/JOE-08-0205. Epub 2008 May 20.