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非酒精性脂肪性肝病患者血清和肝组织胰腺衍生因子水平变化及意义
引用本文:杨帆,李良平.非酒精性脂肪性肝病患者血清和肝组织胰腺衍生因子水平变化及意义[J].实用肝脏病杂志,2014(5):479-483.
作者姓名:杨帆  李良平
作者单位:电子科技大学医学院附属四川省人民医院消化科,成都市610072
摘    要:目的研究胰腺衍生因子(PANDER)在非酒精性脂肪性肝病(NAFLD)患者血清和肝组织的水平。方法纳入经肝组织病理学活检证实的NAFLD患者41例,以及20例正常人(NC),根据NAFLD活动性积分(NAS),将NAFLD患者分为单纯性脂肪肝(NAFL)10例和非酒精性脂肪性肝炎(NASH)31例。采用ELISA法检测受试者血清和肝组织PANDER水平;采用实时荧光定量PCR法检测肝组织PANDER mRNA水平的变化。另外,收集所有研究对象的人体测量学、生化及代谢指标,分别比较PANDER水平及与其相关性。结果 NAFLD患者血清PANDER水平为(3.38±1.99)ng/ml,较NC组(0.94±0.60)ng/ml]升高,差异有统计学意义(P〈0.05);NAFLD患者肝组织PANDER水平为(3.27±2.49)ng/ml,显著高于NC组(0.98±0.73)ng/ml,P〈0.05];NAFL组和NASH组血清PANDER水平分别为(3.42±2.39)ng/ml和(3.36±1.91)ng/ml,肝组织PANDER水平分别为(2.33±1.52)ng/ml和(3.58±2.68)ng/ml,差异无统计学意义;血清PANDER与肝组织PANDER水平、BMI、腰围、臀围、TG、FBG、FINS、HMOA-IR的相关系数分别0.425、0.643、0.637、0.375、0.411、0.487、0.512和0.547,均呈正相关关系(P〈0.05),与IAI(r=-0.544)、HDL-C(r=-0.396)呈负相关(P〈0.05);肝组织PANDER水平与血清PANDER水平、BMI和腰围的相关系数分别为0.425、0.379和0.427,也呈正相关(P〈0.05)。结论 PANDER可能通过影响胰岛素抵抗和糖脂代谢参与NAFLD的发生与发展。

关 键 词:非酒精性脂肪性肝病  胰腺衍生因子  胰岛素抵抗  脂质  糖代谢

Serum and hepatic level of pancreatic derived factor in patients with non-alcoholic fatty liver diseases
Institution:Yang Fan,Li Liannping.( Department of Gastroenterology,Provincial People's Hospital,Chengdu 610072,Sichuan ProVince, China)
Abstract:Objective To explore the serum and hepatic level of pancreatic derived factor(PANDER) in patients with non-alcoholic fatty liver diseases(NAFLD). Methods Forty-one patients with NAFLD confirmed by liver biopsy and 20 healthy persons were included in this study and the patients with NAFLD were further divided into NAFL group(n=10) and NASH group(n=31 cases) according to the NAFLD activity score(NAS).Serum and hepatic level of PANDER were detected by ELISA method and hepatic level of PANDER mRNA was determined by real-time PCR. Anthropometry data,biochemical and metabolic parameters of all subjects were collected and compared between different groups. Results The serum level and hepatic level of PANDER in patients with NAFLD were(3.38±1.99) ng/ml and(3.27±2.49) ng/ml,respectively,significantly higher than those in healthy controls (0.94±0.60) ng/ml,(0.98±0.73) ng/ml),respectively,P〈0.05];No significant difference in serum level (3.42±2.39) ng/ml vs.(3.36±1.91) ng/ml] and hepatic level (2.33±1.52) ng/ml vs.(3.58±2.68) ng/ml] of PANDER between patients with NAFL and NASH;Serum level of PANDER were positively correlated with hepatic level of PANDER(r =0.425),BMI(r =0.643),waist circumference(r =0.637),hip circumference(r =0.375,triglyceride(r=0.411),fasting blood glucose(r=0.487),fasting insulin(r=0.512) and homeostasis model assessment index(HOMA-IR,r=0.547,P〈0.05),and negatively correlated with insulin action index(r=-0.544) and high-density lipoprotein cholesterol(r =-0.396,P 0.05). Hepatic level of PANDER were positively correlated with serum PANDER level(r=0.425),body mass index(r=0.379) and waist circumference(r=0.427,P〈0.05). Conclusion PANDER plays an important role in the pathogenesis of NAFLD by affecting body insulin resistance and glucose and lipid metabolisms.
Keywords:Nonalcoholic fatty liver diseases  Pancreatic derived factor  Insulin resistance  Lipid  Glucose metabolism
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