Glucocorticoids Increase NPY Gene Expression via Hypothalamic AMPK Signaling in Broiler Chicks
Author(s) -
Lei Liu,
Zhigang Song,
Hongchao Jiao,
Hai Lin
Publication year - 2014
Publication title -
endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.674
H-Index - 257
eISSN - 1945-7170
pISSN - 0013-7227
DOI - 10.1210/en.2013-1632
Subject(s) - ampk , endocrinology , medicine , neuropeptide y receptor , protein kinase a , appetite , receptor , signal transduction , neuropeptide , chemistry , mifepristone , amp activated protein kinase , glucocorticoid , phosphorylation , biology , biochemistry , pregnancy , genetics
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.
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