Hu Xiyi, Kong Linglian, Xiao Chuanpi, Zhu Qidong, Song Zhigang
Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271018, China.
Department of Animal Science, Shandong Agricultural University, Taian, Shandong 271018, China; Precision Livestock and Nutrition Unit, Gembloux Agro-Bio Tech, University of Liège, Gembloux 5030, Belgium.
Comp Biochem Physiol A Mol Integr Physiol. 2021 Aug;258:110979. doi: 10.1016/j.cbpa.2021.110979. Epub 2021 May 12.
Glucocorticoids (GCs) can stimulate the appetite and AMPK in broilers. The activation of hypothalamic mTOR has been proposed as an important anorexigenic signal. However, inhibitory effect of AMPK activity on appetite and AMPK downstream signaling pathway under stress has not been reported. In this study, we performed an intracerebroventricular (icv) injection of compound C, an AMPK inhibitor, in GC-treated birds to explore the regulatory mechanism on appetite and AMPK downstream signaling pathway. A total of 48 7-day-old broilers, which had received an icv cannula, were randomly subjected to one of two treatments: subcutaneous injection of dexamethasone (DEX) or saline. After 3 days of continuous DEX injection, chicks of each group received an icv injection with either compound C (6 μg/2 μL) or vehicle (dimethyl sulfoxide, 2 μL). The results showed that body weight gain was reduced by the DEX treatment. Compared with the control, icv injection of compound C reduced feed intake at 0.5-1.5 h. In the DEX-treated group, the inhibitory effect of compound C on appetite remained apparent at 0.5-1 h. The DEX treatment increased the gene expression of liver kinase B1 (LKB1), neuropeptide Y (NPY), and decreased p-mTOR protein level. In stressed broilers, inhibition of AMPK relieved the decreased mTOR activity. A significant interaction was noted in DEX and compound C on protein expression of phospho-AMPK. Taken together, in stressed broilers, the central injection of compound C could inhibit central AMPK activity and reduce appetite, in which the AMPK/mTOR signaling pathway might be involved.
糖皮质激素（GCs）可刺激肉鸡的食欲并激活其AMPK。下丘脑mTOR的激活被认为是一种重要的厌食信号。然而，应激状态下AMPK活性对食欲及AMPK下游信号通路的抑制作用尚未见报道。在本研究中，我们对经GC处理的肉鸡进行脑室内（icv）注射化合物C（一种AMPK抑制剂），以探究其对食欲及AMPK下游信号通路的调节机制。共有48只接受了icv插管的7日龄肉鸡，随机接受两种处理之一：皮下注射地塞米松（DEX）或生理盐水。连续注射DEX 3天后，每组雏鸡接受icv注射化合物C（6μg/2μL）或溶剂（二甲基亚砜，2μL）。结果显示，DEX处理使体重增加减少。与对照组相比，icv注射化合物C使0.5 - 1.5小时的采食量降低。在DEX处理组中，化合物C对食欲的抑制作用在0.5 - 1小时仍很明显。DEX处理使肝脏激酶B1（LKB1）、神经肽Y（NPY）的基因表达增加，使p - mTOR蛋白水平降低。在应激的肉鸡中，抑制AMPK可缓解mTOR活性的降低。DEX与化合物C对磷酸化AMPK蛋白表达存在显著交互作用。综上所述，在应激的肉鸡中，脑室内注射化合物C可抑制中枢AMPK活性并降低食欲，其中可能涉及AMPK/mTOR信号通路。
