Visfatin、锌-α2糖蛋白在NAFLD发病机制中的研究进展

Role of visfatin and zinc-α2-glycoprotein in pathogenesis of non-alcoholic fatty liver disease

内脏脂肪素(visfatin)是一种新的脂肪因子,于2005年被Fukuhara等发现高度富集在人类和小鼠的内脏脂肪,之前被称为前B细胞集落增强因子(pre-B-cell colony-enhancing factor,PBEF),表现出烟酰胺磷酸酶(nicotinamide phosphoribosyl transferase,Nampt)的活性,并具有调节β细胞分泌胰岛素作用,研究显示其与非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)有密切的关系;锌-α2糖蛋白(zinc-α2-glycoprotein,ZAG)是一种从人类血浆中分离出来的单链多肽,以前称为脂质动员因子(lipid-mobilising factor,LMF),他是由褐色和白色脂肪细胞分泌的脂肪因子.ZAG可能作为一种新的蛋白因子在组织内影响脂质的分解,同时其与非酒精性脂肪性肝病也有着密切关系.本文综述了visfatin、ZAG在NAFLD发病机制中作用研究进展.

Visfatin is a novel adipokine which was discovered in 2005 by Fukuhara. Visfatin is highly enriched in the visceral fat of humans and mice with obesity, which was previously called pre-B-cell colony- enhancing factor, and exhibits nicotinamide phosphoribosyl transferase enzymatic activity. Visfatin regulates insulin secretion in pancreatic cells. Visfatin is not only an adipocyte-specific protein, and it has a close relation with non- alcoholic fatty liver disease （NAFLD）. Zinc-α2- glycoprotein （ZAG）, which is identical to the previously named lipid-mobilising factor, is a single-chain polypeptide. It is secreted by both brown and white adipocytes. ZAG possibly functions as a novel protein factor responsible for the decomposition of tissue lipids. ZAG also has a close relationship with NAFLD. This paper will review the advances in understanding the role of visfatin and ZAG in the pathogenesis of NAFLD.