Glucocorticoids (GCs) induce profound hyperphagia in birds. However, the neuronal regulatory network underlying GC-provoked hyperphagia is unclear. To determine whether any cross talk occurs among hypothalamic GC receptors (GRs), AMP-activated protein kinase (AMPK), and GCs in the regulation of appetite, we performed an intracerebroventricular injection of mifepristone (a GR inhibitor) and compound C (an AMPK inhibitor) on GC-treated male chicks. The results indicate that central GC administration increased the expression of GR and neuropeptide Y mRNA, as well as phosphorylated AMPKαThr172 and acetyl-coenzyme A carboxylaseSer79. Blocking AMPK significantly attenuated GC-induced hyperphagia. BlockingGRsignificantly attenuated part of theAMPK signaling pathway and GC-induced hyperphagia. Thus, the results suggest that GCs cause hyperphagia via the AMPK-neuropeptide Y signaling pathway. Copyright © 2014 by the Endocrine Society.
CITATION STYLE
Liu, L., Song, Z., Jiao, H., & Lin, H. (2014). Glucocorticoids increase NPY gene expression via hypothalamic AMPK signaling in broiler chicks. Endocrinology, 155(6), 2190–2198. https://doi.org/10.1210/en.2013-1632
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