Glucocorticoids increase NPY gene expression via hypothalamic AMPK signaling in broiler chicks.
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 AMPKα(Thr172) and acetyl-coenzyme A carboxylase(Ser79). Blocking AMPK significantly attenuated GC-induced hyperphagia. Blocking GR significantly attenuated part of the AMPK signaling pathway and GC-induced hyperphagia. Thus, the results suggest that GCs cause hyperphagia via the AMPK-neuropeptide Y signaling pathway.
Department of Animal Science, Shandong Agricultural University, Shandong Key Laboratory for Animal Biotechnology and Disease Control, Taian, Shandong 271018, China.
Lei
L
Liu
Zhigang
Z
Song
Hongchao
H
Jiao
Hai
H
Lin
D055372:AMP-Activated Protein Kinases / Q000378:metabolism*; D000818:Animals; D004435:Eating / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects*; D005938:Glucocorticoids / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D009478:Neuropeptide Y / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*
D005938:Glucocorticoids; D009478:Neuropeptide Y; D055372:AMP-Activated Protein Kinases