Lipopolysaccharide inhibits hypothalamic Agouti-related protein gene expression via activating mechanistic target of rapamycin signaling in chicks

• Published in: General and comparative endocrinology Vol. 313; p. 113876
• Main Authors: Wang, X.J., Li, D., Jiao, H.C., Zhao, J.P., Lin, H.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2021
• Subjects: Agouti-Related Protein - genetics; AgRP; Appetite control; Chick; Gene Expression; Lipopolysaccharide; Lipopolysaccharides - toxicity; mTOR; Signal Transduction; Sirolimus - pharmacology; TOR Serine-Threonine Kinases; Lipopolysaccharide; mTOR; AgRP; Chick; Appetite control
• ISSN: 0016-6480; 1095-6840
• DOI: 10.1016/j.ygcen.2021.113876

•LPS induce chick anorexia via hypothalamic mTOR-AgRP signaling.•mTOR signaling is associated with the regulation of LPS in p-NF-кB. Lipopolysaccharide (LPS) induces profound anorexia in birds. However, the neuronal regulatory network underlying LPS-provoked anorexia is unclear. To determine whether any cross talk occurs among hypothalamic mechanistic target of rapamycin (mTOR) and LPS in the regulation of appetite, we performed an intracerebroventricular injection of rapamycin (an mTOR inhibitor) on LPS-treated chicks. The results indicate that peripheral administrations of LPS decreased the agouti-related protein (AgRP) mRNA level, but increased the phosphorylated mTOR and nuclear factor-кB (NF-кB) protein level. Blocking mTOR significantly attenuated LPS-induced anorexia, AgRP suppression, and p-NF-кB increase. Thus, the results suggest that LPS causes anorexia via the mTOR-AgRP signaling pathway, and mTOR signaling is also associated with the regulation of LPS in p-NF-кB.