College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P.R. China.
Animal Production Research Institute, Agricultural Research Centre, Giza, Egypt.
J Anim Sci. 2022 Sep 1;100(9). doi: 10.1093/jas/skac244.
In the modern poultry industry, newly hatched chicks are unavoidably transported from the hatching to the rearing foster. Stress caused by multiple physical and psychological stressors during transportation is particularly harmful to the liver. Astragalus polysaccharide (APS) possesses multiple benefits against hepatic metabolic disorders. Given that transport stress could disturb hepatic glucolipid metabolism and the role of APS in metabolic regulation, we speculated that APS could antagonize transport stress-induced disorder of hepatic glucolipid metabolism. Firstly, newly hatched chicks were transported for 0, 2, 4, and 8 h, respectively. Subsequently, to further investigate the effects of APS on transport stress-induced hepatic glucolipid metabolism disturbance, chicks were pretreated with water or APS and then subjected to transport treatment. Our study suggested that APS could relieve transport stress-induced lipid deposition in liver. Meanwhile, transport stress also induced disturbances in glucose metabolism, reflected by augmented mRNA expression of key molecules in gluconeogenesis and glycogenolysis. Surprisingly, APS could simultaneously alleviate these alterations via peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α)/Sirtuin 1 (SIRT1)/AMP-activated protein kinase (AMPK) pathway. Moreover, APS treatment regulated the level of peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma (PPARγ), thereby alleviating transport stress-induced alterations of VLDL synthesis, cholesterol metabolism, lipid oxidation, synthesis, and transport-related molecules. These findings indicated that APS could prevent the potential against transport stress-induced hepatic glucolipid metabolism disorders via PGC-1α/SIRT1/AMPK/PPARα/PPARγ signaling system.
在现代家禽养殖业中,刚孵化的小鸡不可避免地要从孵化场运输到饲养场。在运输过程中,多种生理和心理应激源引起的应激对肝脏尤其有害。黄芪多糖(APS)具有多种防治肝代谢紊乱的作用。鉴于运输应激会干扰肝糖脂代谢,而 APS 在代谢调节中的作用,我们推测 APS 可以拮抗运输应激引起的肝糖脂代谢紊乱。首先,将刚孵化的小鸡分别运输 0、2、4 和 8 h。随后,为了进一步研究 APS 对运输应激引起的肝糖脂代谢紊乱的影响,将小鸡用生理盐水或 APS 预处理,然后进行运输处理。我们的研究表明,APS 可以缓解运输应激引起的肝脏脂质沉积。同时,运输应激也导致葡萄糖代谢紊乱,表现为糖异生和糖原分解关键分子的 mRNA 表达增加。令人惊讶的是,APS 可以通过过氧化物酶体增殖物激活受体γ共激活因子 1α(PGC-1α)/沉默调节蛋白 1(SIRT1)/腺苷酸活化蛋白激酶(AMPK)途径同时缓解这些变化。此外,APS 处理调节过氧化物酶体增殖物激活受体α(PPARα)和过氧化物酶体增殖物激活受体γ(PPARγ)的水平,从而缓解运输应激引起的 VLDL 合成、胆固醇代谢、脂质氧化、合成和转运相关分子的改变。这些发现表明,APS 可以通过 PGC-1α/SIRT1/AMPK/PPARα/PPARγ信号系统预防潜在的运输应激引起的肝糖脂代谢紊乱。