Zinc alpha2 glycoprotein alleviates palmitic acid-induced intracellular lipid accumulation in hepatocytes.
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 β-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 β-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.
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Xinhua
X
Xiao
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Han
H
Li
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Xiaoyan
X
Qi
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Yadi
Y
Wang
Department of Pathology & Immunology, Developmental, Regenerative and Stem Cell Biology, Washington University in St. Louis, MO, 63110, United States.
Canxin
C
Xu
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Gexin
G
Liu
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China.
Gebo
G
Wen
Department of Metabolism and Endocrinology, The First Affiliated Hospital of University of South China, 421001, People's Republic of China. Electronic address: jianghua990@163.com.
Jianghua
J
Liu
D052242:Adiponectin / Q000378:metabolism; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D042541:Intracellular Space / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects*; D050155:Lipogenesis / Q000187:drug effects; D010084:Oxidation-Reduction / Q000187:drug effects; D047493:PPAR alpha / Q000378:metabolism; D019308:Palmitic Acid / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D029589:Seminal Plasma Proteins / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects; D000090203:Zn-Alpha-2-Glycoprotein; D000099150:Receptor, Farnesoid X-Activated
D052242:Adiponectin; D047493:PPAR alpha; D019308:Palmitic Acid; D012333:RNA, Messenger; D018160:Receptors, Cytoplasmic and Nuclear; D029589:Seminal Plasma Proteins; D000090203:Zn-Alpha-2-Glycoprotein; D000099150:Receptor, Farnesoid X-Activated
Adiponectin; Fatty acid oxidation; Lipogenesis; Non-alcoholic fatty liver disease; Nuclear receptors; Triglycerides