Hu Ying-Xiu, Liang QiuYang, Li Ang, Bai Ding-Ping
Fujian Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health, College of Animal Sciences, Fujian Agricultural and Forestry University, Fuzhou 350002, China.
Fujian Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health, College of Animal Sciences, Fujian Agricultural and Forestry University, Fuzhou 350002, China.
Poult Sci. 2024 Dec;103(12):104268. doi: 10.1016/j.psj.2024.104268. Epub 2024 Aug 28.
Mule ducks accumulate a large amount of fat in their livers when fed high-energy feed, which is predominantly used for producing fatty livers. Nevertheless, there is limited research on the molecular mechanisms underlying the formation of fatty liver in mule ducks. Fatty acid translocase (CD36) is a sensor for fatty acids and lipid metabolism regulator, which may play a crucial role in the accumulation of fat in the liver of mule ducks. In this study, Overexpression and CD36 gene interference for 24 h was followed by induction of liver cells with 400 µmol/L palmitic acid (PA) for 24 h. The results demonstrated that CD36 overexpression increased hepatic triglyceride content, lipid droplet deposition, oxidative stress, and cell apoptosis. However, interference with CD36 had the opposite effect. CD36 overexpression suppressed the expression of AMPK and CPT-1A genes but enhanced the expression of ACC1 and LKB1 genes, with interference yielding contrasting results. Additionally, the expression of CD36 inhibited the AMPK pathway, reduced AMPK phosphorylation, downregulated AMPK protein expression, and upregulated SREBP1 protein expression. This promoted palmitic acid-induced hepatocyte fat accumulation. In summary, CD36 promotes palmitic acid-induced fat accumulation in primary mule duck liver cells through the AMPK signaling pathway.
骡鸭在饲喂高能饲料时，其肝脏会积累大量脂肪，这些脂肪主要用于生产肥肝。然而，关于骡鸭脂肪肝形成的分子机制的研究有限。脂肪酸转运蛋白（CD36）是一种脂肪酸传感器和脂质代谢调节因子，可能在骡鸭肝脏脂肪积累中起关键作用。在本研究中，对肝细胞进行CD36基因过表达和干扰24小时后，用400µmol/L棕榈酸（PA）诱导肝细胞24小时。结果表明，CD36过表达增加了肝脏甘油三酯含量、脂滴沉积、氧化应激和细胞凋亡。然而，干扰CD36则产生相反的效果。CD36过表达抑制了AMPK和CPT-1A基因的表达，但增强了ACC1和LKB1基因的表达，干扰则产生相反的结果。此外，CD36的表达抑制了AMPK途径，降低了AMPK磷酸化，下调了AMPK蛋白表达，并上调了SREBP1蛋白表达。这促进了棕榈酸诱导的肝细胞脂肪积累。总之，CD36通过AMPK信号通路促进棕榈酸诱导的原代骡鸭肝细胞脂肪积累。
