非酒精性脂肪性肝病患者血清SFRP5水平与血脂相关性分析

发布时间：2018-08-19 07:32

【摘要】：背景：非酒精性脂肪性肝病(Non-alcoholic fatty liver disease, NAFLD)是除外酒精和其它明确的肝损害因素所致的,以肝脏细胞内脂肪变为主要特征的慢性肝脏疾病,一逐渐成为我国及西方国家常见的慢性肝脏疾病。分泌型卷曲相关蛋白5(Secreted frizzled-related protein 5, SFRP5)是一种能内源性抑制Wnt信号通路的抗炎脂肪因子,近年来SFRP5在许多代谢性疾病如2型糖尿病、肥胖、冠心病中的表达及意义均有较多研究。越来越多的研究表明NAFLD与肥胖、2型糖尿病、胰岛素抵抗、高脂血症、心血管疾病密切相关,而SFRP5在NAFLD中的表达情况及其与血脂等因素的相关性国内外尚无相关研究。目的：探讨SFRP5在非酒精性脂肪性肝病血清中的表达水平及其与血脂等相关影响因素的关系。方法；收集2013年10月-2014年7月重庆医科大学附属第二医院诊断为NAFLD患者58人作为实验组,体检中心健康体检者58人作为对照组(NC),根据腹部超声表现由有经验的两名超声科医生将肝脏脂肪变程度分为轻、中、重度,根据脂肪变程度将NAFLD组分为三亚组。于重庆医科大学附属第二医院检验科测定空腹血糖(FastingPlasma Glucose, FPG)、糖化血红蛋白(HBAlc)、总胆固醇(Total Cholesterol, TC)、甘油三酯(Triglyceride, TG)、高密度脂蛋白(High-density lipoprotein, HDL)、低密度脂蛋白(Low density lipoprotein, LDL)、游离脂肪酸(Free fatty acid, FFA)、载脂蛋白B (Apolipoprotein B, ApoB)、尿酸(Uricacid)、谷丙转氨酶(Alanine aminotransf erase, ALT)、谷草转氨酶(Aspartate aminotransf erase,AST)、碱性磷酸酶(Alkaline phosphatase, ALP)、谷氨酰转肽酶(Gamma-glutamyl transpeptidase, y -GGT)、总胆红素(Total bilirubin, TB)、结合胆红素(Conjugated bilirubin, CB)、非结合胆红素(Unconjugated bilirubin, UCB)、凝血酶原活动度(Prothrombin activity, PTA)水平；采用ELISA法检测血清SFRP5水平,分析NAFLD患者中SFRP5与血脂及其他影响因素的相关性。结果：与NC组相比,NAFLD组的BMI、SBP、DBP、HbA1c、TG、TC、LDL-C, ApoB、Uric acid、ALT、AST、γ-GGT, SFRP5水平明显升高(P0.05或P0.01,)；Pearson相关分析显示,血清SFRP5与TC、HDL-C、ApoB呈负相关性(P0.05或P0.01)；Spearman相关分析显示,血清SFRP5与肝脏脂肪变呈正相关性(P=0.029,r=0.287)；多元线性回归显示,TC是SFRP5的独立影响因素。结论：SFRP5在非酒精性脂肪性肝病中升高且与肝脏脂肪变呈正相关性,与TC呈负相关,提示在对抗肝脏脂肪沉积、代谢应激、胰岛素抵抗等存在急性或慢性代偿机制,可能参与延缓非酒精脂肪性肝病的发展。
[Abstract]:BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by intracellular fatty degeneration of the liver, which is caused by alcohol and other specific liver damage factors. It has gradually become a common chronic liver disease in China and Western countries. Secret-related protein 5 (Secret-5) Ed frizzled-related protein 5 (SFRP5) is an endogenous anti-inflammatory adipokine that inhibits the Wnt signaling pathway. In recent years, the expression and significance of SFRP5 in many metabolic diseases such as type 2 diabetes mellitus, obesity, coronary heart disease have been studied. Objectives: To investigate the expression of SFRP5 in non-alcoholic fatty liver disease (NAFLD) serum and its relationship with blood lipids and other related factors. Fifty-eight patients with NAFLD diagnosed in the Second Affiliated Hospital of the University were selected as the experimental group and 58 healthy people as the control group (NC). According to the abdominal ultrasound findings, two experienced ultrasound doctors divided the degree of liver fatty degeneration into mild, moderate and severe groups. The NAFLD group was divided into three subgroups according to the degree of fatty degeneration. Fasting plasma Glucose (FPG), glycosylated hemoglobin (HBAlc), total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), free fatty acid (FFA), were measured in the Laboratory Department of the Second Hospital. Apolipoprotein B (ApoB), Uricacid, Alanine aminotransf erase (ALT), Aspartate aminotransf erase (AST), Alkaline phosphatase (ALP), Gamma-glutamyl transpeptidase (y-GGT), Total bilirubin (TB), and Binding Bile Conjugated bilirubin (CB), Unconjugated bilirubin (UCB) and prothrombin activity (PTA) were measured. Serum SFRP5 levels were measured by ELISA to analyze the correlation between SFRP5 and blood lipids and other influencing factors in NAFLD patients. Results: Compared with NC group, BMI, SBP, DBP, HbA1c, TG in NAFLD group were detected. TC, LDL-C, ApoB, Uric acid, ALT, AST, gamma-GGT, SFRP5 levels significantly increased (P 0.05 or P 0.01,); Pearson correlation analysis showed that serum SFRP5 and TC, HDL-C, ApoSpearman correlation analysis showed that serum SFRP5 and liver steatosis were positively correlated (P = 0.029, r = 0.287); multiple linear regression analysis showed that SFRP5 was a negative correlation (P 0.05 or P 0.01); serum SFRP5 was positively correlated with liver steatosis (P = 0.029, r = 0.287). Conclusion: SFRP5 is elevated in non-alcoholic fatty liver disease and positively correlated with hepatic steatosis, and negatively correlated with TC, suggesting that there are acute or chronic compensatory mechanisms against liver fat deposition, metabolic stress and insulin resistance, which may be involved in delaying the development of non-alcoholic fatty liver disease.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R575.5

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