Zinc alpha2 glycoprotein alleviates palmitic acid-induced intracellular lipid accumulation in hepatocytes
Zinc alpha2 glycoprotein alleviates palmitic acid-induced intracellular lipid accumulation in hepatocytes
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DOI：
10.1016/j.mce.2016.06.003
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发表时间：
2017-01-05
影响因子：
4.1
通讯作者：
Liu, Jianghua
中科院分区：
文献类型：
--
作者：
Xiao, Xinhua;Li, Han;Liu, Jianghua
锌α 2糖蛋白（ZAG）在刺激脂肪组织的脂肪动员和脂解中起重要作用，但其在肝脏脂质代谢中的作用尚不清楚。使用棕榈酸（PA）刺激具有ZAG过表达或ZAG敲低（shRNA）的HepG 2细胞。ZAG的过表达显著抑制脂肪生成，促进脂解和脂肪酸β-氧化，并减弱PA诱导的细胞内脂肪积累。此外，ZAG过表达显著刺激HepG 2细胞中脂联素的表达。相反，ZAG的敲低显著抑制脂肪酸β-氧化，增加脂肪生成和脂质积累。总的来说，这些数据表明，ZAG具有缓解脂肪肝的潜力，使其成为脂肪肝的有希望的治疗靶点。(C)由Elsevier爱尔兰Ltd.出版
Zinc alpha2 glycoprotein (ZAG) plays an important role in stimulating fat mobilization and lipolysis in adipose tissue, but its role in hepatic lipid metabolism remains unclear. Palmitic acid (PA) was used to stimulate HepG2 cells with ZAG overexpression or ZAG knock down (shRNA). Overexpression of ZAG significantly inhibited lipogenesis, promoted lipolysis and fatty acid beta-oxidation, and attenuated PA induced intracellular fat accumulation. Moreover, ZAG overexpression dramatically stimulated adiponectin expression in HepG2 cells. In contrast, knockdown of ZAG notably inhibited fatty acid beta-oxidation, increased lipogenesis and lipid accumulation. Collectively, these data suggest that ZAG has the potential to alleviate hepatosteatosis, making it a promising therapeutic target for fatty liver. (C) 2016 Published by Elsevier Ireland Ltd.