Inducible-NOS but not neuronal-NOS participate in the acute effect of TNF-α on hypothalamic insulin-dependent inhibition of food intake

18Citations
Citations of this article
15Readers
Mendeley users who have this article in their library.

Abstract

TNF-α acts on the hypothalamus modulating food intake and energy expenditure through mechanisms incompletely elucidated. Here, we explore the hypothesis that, to modulate insulin-induced anorexigenic signaling in hypothalamus, TNF-α requires the synthesis of NO. TNF-α activates signal transduction through JNK and p38 in hypothalamus, peaking at 10-8 M. This is accompanied by the induction of expression of the inducible and neuronal forms of NOS, in both cases peaking at 10-12 M. In addition, TNF-α stimulates NOS catalytic activity. Pre-treatment with TNF-α at a low dose (10-12 M) inhibits insulin-dependent anorexigenic signaling, and this effect is abolished in iNOS but not in nNOS knockout mice. © 2006 Federation of European Biochemical Societies.

Cite

CITATION STYLE

APA

Moraes, J. C., Amaral, M. E., Picardi, P. K., Calegari, V. C., Romanatto, T., Bermúdez-Echeverry, M., … Velloso, L. A. (2006). Inducible-NOS but not neuronal-NOS participate in the acute effect of TNF-α on hypothalamic insulin-dependent inhibition of food intake. FEBS Letters, 580(19), 4625–4631. https://doi.org/10.1016/j.febslet.2006.07.042

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free