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zinc-α2-glycoprotein 1 attenuates non-alcoholic fatty liver disease by negatively regulating tumour necrosis factor-α

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World Journal of Gastroenterology 2019年第36期25卷 5451-5468页

作者： Ting Liu Xin Luo Zheng-Hong Li Jun-Cheng Wu Sheng-Zheng Luo Ming-Yi Xu Department of Gastroenterology Shanghai General Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200080 China Department of Gastroenterology The Second Hospital of Hebei Medical University Shijiazhuang 050000 Hebei Province China Shanghai Key Laboratory of Pancreatic Diseases Shanghai General Hospital Shanghai Jiao Tong University School of Medicine Shanghai 200080 China

BACKGROUND zinc-α2-glycoprotein 1 (AZGP1) plays important roles in metabolism-related diseases. The underlying molecular mechanisms and therapeutic effects of AZGP1 remain unknown in non-alcoholic fatty liver disease (NAFLD). AIM To explore the effects and potential mechanism of AZGP1 on NAFLD in vivo and in vitro. METHODS The expression of AZGP1 and its effects on hepatocytes were examined in NAFLD patients, CCl4-treated mice fed a high fat diet (HFD), and human LO2 cells. RESULTS AZGP1 levels were significantly decreased in liver tissues of NAFLD patients and mice. AZGP1 knockdown was found to activate inflammation;enhance steatogenesis, including promoting lipogenesis [sterol regulatory elementbinding protein (SREBP)-1c, liver X receptor (LXR), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl CoA desaturase 1 (SCD)-1], increasing lipid transport and accumulation [fatty acid transport protein (FATP), carnitine palmitoyl transferase (CPT)-1A, and adiponectin], and reducing fatty acid β-oxidation [farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor (PPAR)-α];accelerate proliferation;and reverse apoptosis in LO2 cells. AZGP1 overexpression (OV-AZGP1) had the opposite effects. Furthermore, AZGP1 alleviated NAFLD by blocking TNF-α-mediated inflammation and intracellular lipid deposition, promoting proliferation, and inhibiting apoptosis in LO2 cells. Finally, treatment with OV-AZGP1 plasmid dramatically improved liver injury and eliminated liver fat in NAFLD mice. CONCLUSION AZGP1 attenuates NAFLD with regard to ameliorating inflammation, accelerating lipolysis, promoting proliferation, and reducing apoptosis by negatively regulating TNF-α. AZGP1 is suggested to be a novel promising therapeutic target for NAFLD.

关键词： Non-alcoholic fatty liver disease zinc-α2-glycoprotein 1 Tumour necrosis factor-α Inflammation Lipid metabolism

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Expression and Function of zinc-α2-glycoprotein

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Neuroscience Bulletin 2019年第3期35卷 540-550页

作者： Xin Wei Xi Liu Changhong Tan Lijuan Mo Hui Wang Xi Peng Fen Deng Lifen Chen Department of Neurology The Second Affiliated Hospital of Chongqing Medical University

zinc-α2-glycoprotein(ZAG), encoded by the AZGP1 gene, is a major histocompatibility complex I molecule and a lipid-mobilizing factor. ZAG has been demonstrated to promote lipid metabolism and glucose utilization, and to regulate insulin sensitivity. Apart from adipose tissue, skeletal muscle, liver, and kidney, ZAG also occurs in brain tissue, but its distribution in brain is debatable. Only a few studies have investigated ZAG in the brain. It has been found in the brains of patients with Krabbe disease and epilepsy, and in the cerebrospinal fluid of patients with Alzheimer disease, frontotemporal lobe dementia, and amyotrophic lateral sclerosis. Both ZAG protein and AZGP1 m RNA are decreased in epilepsy patients and animal models, while overexpression of ZAG suppresses seizure and epileptic discharges in animal models of epilepsy, but knowledge of the specific mechanism of ZAG in epilepsy is limited. In this review, we summarize the known roles and molecular mechanisms of ZAG in lipid metabolism and glucose metabolism, and in the regulation of insulin sensitivity, and discuss the possible mechanisms by which it suppresses epilepsy.

关键词： zinc-α2-glycoprotein Metabolism Glucose Lipid Insulin sensitivity Neuron

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Fatty Acid Synthase and Hormone-sensitive Lipase Expression in Liver Are Involved in zinc-α2-glycoprotein-induced Body Fat Loss in Obese Mice

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Chinese Medical Sciences Journal 2010年第3期25卷 169-175页

作者： Feng-ying Gong Jie-ying Deng Hui-juan Zhu Hui Pan Lin-jie Wang Hong-bo Yang Department of Endocrinology Key Laboratory of Endocrinology of Ministry of Health Peking Union Medical College Hospital Chinese Academy of Medical Sciences ＆ Peking Union Medical College Beijing 100730 China

Objective To explore the effects of zinc-0t2-glycoprotein （ZAG） on body weight and body fat in high-fat-diet （HF1））-induced obesity in mice and the possible mechanism. Methods Thirty-six male mice were fed with standard food （SF）（n=9） and HFD （n=27）, respectively. Five weeks later, 9 mice fed with HFD were subjected to ZAG expression plasmid DNA transfection by liposome transfection method, and another 9 mice to negative control plasmid transfection. Two weeks later, serum ZAG level in the mice was assayed by Western blot, and the effects of ZAG over-expression on body weight, body fat, serum biochemical indexes, and adipose tissue of obese mice were evaluated. The mRNA expressions of fatty acid synthase （FAS） and hormone sensitive lipase （HSL） in liver tissue were deterlnined by reverse transcription-polymerase chain reaction. Results Serum ZAG level significantly lowered in simple HFD-fed mice in comparison to SF-fed mice （0.51±0.10 AU vs. 0.75±0.07 AU, P〈0.01）. Further statistical analysis demonstrated that ZAG level was negatively correlated with body weight （r =-0.56, P〈0.001）, epididymal fat mass （r=-0.67, P〈O. 001）, percentage of epididymal fat （r= 0.65, P〈0.001）, and increased weight （r= 0.57, P〈0.001） in simple SF- and HFD fed mice. ZAG over-expression in obese mice reduced body weight and the percentage of epididyreal fat. Furthermore, FAS mRNA expression decreased （P〈0.01） and HSL mRNA expression increased （P〈0.001） in the liver in ZAG over-expressing mice. Conclusions ZAG is closely related to obesity. Serum ZAG level is inversely correlated with body weight and percentage of body fat. The action of ZAG is associated with reduced FAS expression and increased HSL expression in the liver of obese mice.

关键词： zinc-α2-glycoprotein adipose tissue fatty acid synthase hormone-sensitivelipase obesity

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2型糖尿病患者血清锌α2糖蛋白水平的变化及其相关因素分析

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中国糖尿病杂志 2012年第2期20卷 102-104页

作者：解婧蒋志华成兴波苏州大学附属第一医院内分泌科 215006 苏州金闾医院

目的探讨T2DM患者血清锌α2糖蛋白(ZAG)的水平与胰岛素抵抗(IR)的相关性,探索其潜在的作为肥胖或代谢综合征血清指标的可能性。方法 166名受试者分为T2DM组和正常糖耐量(NGT)组,根据BMI又分为正常体重组(NW)和超重肥胖组(OW-OB)两个亚组... 详细信息

目的探讨T2DM患者血清锌α2糖蛋白(ZAG)的水平与胰岛素抵抗(IR)的相关性,探索其潜在的作为肥胖或代谢综合征血清指标的可能性。方法 166名受试者分为T2DM组和正常糖耐量(NGT)组,根据BMI又分为正常体重组(NW)和超重肥胖组(OW-OB)两个亚组,均测定空腹血清ZAG水平和相关临床指标。结果 T2DM组比NGT组空腹血清ZAG水平明显升高(t=2.228,P=0.028)。T2DM组患者空腹血清ZAG水平分别与HOMA-IR,WC,HbA1c,TG正相关(r分别为0.543,0.442,0.385,0.437,P2DM组,WC和HDL-C是其的独立影响因素。结论 T2DM患者血清ZAG显著高于NGT患者,超重肥胖和正常体重亚组间差异无统计学意义。T2DM组中ZAG与HOMA-IR,WC,HbA1c,TG正相关,与HDL-C,TNF-α负相关;其中WC和HDL-C是血清ZAG的独立影响因素。

关键词： zinc-α2-glycoprotein 胰岛素抵抗肥胖糖尿病,2型

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