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Tumor necrosis factor‐α activates signal transduction in hypothalamus and modulates the expression of pro‐inflammatory proteins and orexigenic/anorexigenic neurotransmitters
Author(s) -
Amaral Maria E.,
Barbuio Raquel,
Milanski Marciane,
Romanatto Talita,
Barbosa Helena C.,
Nadruz Wilson,
Bertolo Manoel B.,
Boschero Antonio C.,
Saad Mario J. A.,
Franchini Kleber G.,
Velloso Licio A.
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.03857.x
Subject(s) - orexigenic , endocrinology , tumor necrosis factor alpha , medicine , hypothalamus , signal transduction , energy homeostasis , cytokine , socs3 , biology , receptor , microbiology and biotechnology , neuropeptide y receptor , neuropeptide , obesity , stat3
Tumor necrosis factor‐α (TNF‐α) is known to participate in the wastage syndrome that accompanies cancer and severe infectious diseases. More recently, a role for TNF‐α in the pathogenesis of type 2 diabetes mellitus and obesity has been shown. Much of the regulatory action exerted by TNF‐α upon the control of energy stores depends on its action on the hypothalamus. In this study, we show that TNF‐α 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‐1β, interleukin‐6, interleukin‐10 and suppressor of cytokine signalling‐3, respectively. In addition, TNF‐α induces the expression of neurotransmitters involved in the control of feeding and thermogenesis. Thus, TNF‐α may act directly in the hypothalamus inducing a pro‐inflammatory response and the modulation of expression of neurotransmitters involved in energy homeostasis.