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.

脂多糖 (LPS) 在鸟类中引起严重的厌食。然而，LPS 引起的厌食症的神经元调节网络尚不清楚。为了确定雷帕霉素 (mTOR) 的下丘脑机械靶点 (mTOR) 和 LPS 在食欲调节中是否发生任何串扰，我们对 LPS 处理的小鸡进行了脑室内注射雷帕霉素（一种 mTOR 抑制剂）。结果表明，LPS 的外周给药降低了刺鼠相关蛋白 (AgRP) mRNA 水平，但增加了磷酸化 mTOR 和核因子-кB (NF-кB) 蛋白水平。阻断 mTOR 显着减弱 LPS 诱导的厌食、AgRP 抑制和 p-NF-кB 增加。因此，结果表明LPS通过mTOR-AgRP信号通路引起厌食，mTOR信号也与p-NF-кB中LPS的调节有关。