PMID- 16638016
OWN - NLM
STAT- MEDLINE
DCOM- 20060816
LR  - 20111117
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 98
IP  - 1
DP  - 2006 Jul
TI  - Tumor necrosis factor-alpha activates signal transduction in hypothalamus and 
      modulates the expression of pro-inflammatory proteins and orexigenic/anorexigenic 
      neurotransmitters.
PG  - 203-12
AB  - Tumor necrosis factor-alpha (TNF-alpha) is known to participate in the wastage 
      syndrome that accompanies cancer and severe infectious diseases. More recently, a 
      role for TNF-alpha in the pathogenesis of type 2 diabetes mellitus and obesity 
      has been shown. Much of the regulatory action exerted by TNF-alpha upon the 
      control of energy stores depends on its action on the hypothalamus. In this 
      study, we show that TNF-alpha activates canonical pro-inflammatory signal 
      transduction pathways in the hypothalamus of rats. These signaling events lead to 
      the transcriptional activation of an early responsive gene and to the induction 
      of expression of cytokines and a cytokine responsive protein such as 
      interleukin-1beta, interleukin-6, interleukin-10 and suppressor of cytokine 
      signalling-3, respectively. In addition, TNF-alpha induces the expression of 
      neurotransmitters involved in the control of feeding and thermogenesis. Thus, 
      TNF-alpha may act directly in the hypothalamus inducing a pro-inflammatory 
      response and the modulation of expression of neurotransmitters involved in energy 
      homeostasis.
FAU - Amaral, Maria E
AU  - Amaral ME
AD  - Department of Internal Medicine, State University of Campinas, Sao Paulo, Brazil.
FAU - Barbuio, Raquel
AU  - Barbuio R
FAU - Milanski, Marciane
AU  - Milanski M
FAU - Romanatto, Talita
AU  - Romanatto T
FAU - Barbosa, Helena C
AU  - Barbosa HC
FAU - Nadruz, Wilson
AU  - Nadruz W
FAU - Bertolo, Manoel B
AU  - Bertolo MB
FAU - Boschero, Antonio C
AU  - Boschero AC
FAU - Saad, Mario J A
AU  - Saad MJ
FAU - Franchini, Kleber G
AU  - Franchini KG
FAU - Velloso, Licio A
AU  - Velloso LA
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060421
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Cytokines)
RN  - 0 (Insulin)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Behavior, Animal
MH  - Blotting, Western/methods
MH  - Cytokines/genetics/*metabolism
MH  - Drug Interactions/physiology
MH  - Eating/drug effects
MH  - Gene Expression Regulation/*drug effects
MH  - Genes, Reporter/physiology
MH  - Hypothalamus/*drug effects/metabolism
MH  - Injections, Intraventricular/methods
MH  - Insulin/pharmacology
MH  - Male
MH  - Neurotransmitter Agents/genetics/*metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Signal Transduction/*drug effects
MH  - Transfection/methods
MH  - Tumor Necrosis Factor-alpha/*administration & dosage
EDAT- 2006/04/28 09:00
MHDA- 2006/08/17 09:00
CRDT- 2006/04/28 09:00
PHST- 2006/04/28 09:00 [pubmed]
PHST- 2006/08/17 09:00 [medline]
PHST- 2006/04/28 09:00 [entrez]
AID - JNC3857 [pii]
AID - 10.1111/j.1471-4159.2006.03857.x [doi]
PST - ppublish
SO  - J Neurochem. 2006 Jul;98(1):203-12. doi: 10.1111/j.1471-4159.2006.03857.x. Epub 
      2006 Apr 21.