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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #330216

Research Project: Developmental Determinants of Obesity in Infants and Children

Location: Children's Nutrition Research Center

Title: An indirect action contributes to c-fos induction in paraventricular hypothalamic nucleus by neuropeptide Y

Author
item Fan, Shengjie - Shanghai University
item Dakshinamoorthy, Janani - University Of Texas Medical Branch
item Kim, Eun - University Of Texas Medical Branch
item Xu, Yong - Children'S Nutrition Research Center (CNRC)
item Huang, Cheng - Shanghai University
item Tong, Qingchun - University Of Texas Medical Branch

Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/17/2015
Publication Date: 1/27/2016
Citation: Fan, S., Dakshinamoorthy, J., Kim, E.R., Xu, Y., Huang, C., Tong, Q. 2016. An indirect action contributes to c-fos induction in paraventricular hypothalamic nucleus by neuropeptide Y. Scientific Reports. 6:19980.

Interpretive Summary: Obesity is a serious global health problem. Here we showed that a chemical, Neuropeptide Y (NPY), can strongly promote food intake, and these actions involve activation of a specific brain region. These findings suggest that NPY actions in the brain could be a potential target for treatment of obesity.

Technical Abstract: Neuropeptide Y (NPY) is a well-established orexigenic peptide and hypothalamic paraventricular nucleus (PVH) is one major brain site that mediates the orexigenic action of NPY. NPY induces abundant expression of C-Fos, an indicator for neuronal activation, in the PVH, which has been used extensively to examine the underlying NPY orexigenic neural pathways. However, PVH C-Fos induction is in discordance with the abundant expression of NPY receptors, a group of inhibitory Gi protein coupled receptors in the PVH, and with the overall role of PVH neurons in feeding inhibition, suggesting a mechanism of indirect action. Here we showed that the ability of NPY on C-Fos induction in the PVH was blunted in conditions of insulin deficiency and fasting, a condition associated with a high level of NPY and a low level of insulin. Moreover, insulin insufficiency blunted C-Fos induction in the PVH by fasting-induced re-feeding, and insulin and NPY induced c-Fos induction in the same group of PVH neurons. Finally, NPY produced normal C-Fos induction in the PVH with disruption of GABA-A receptors. Thus, our results revealed that PVH C-Fos induction by NPY is mediated by an indirect action, which is at least partially mediated by insulin action, but not GABA-A receptors.