论文部分内容阅读
目的探讨胰岛素(Insulin)、瘦素(Leptin)及脂联素(Adiponectin)等细胞因子胰岛素抵抗(IR)在非酒精性脂肪肝(NAFLD)发病机理中的作用。方法选择确诊为非酒精性脂肪肝141例(轻度脂肪肝42例;中度脂肪肝51例;重度脂肪肝48例),同时选择40例健康人做对照组。应用酶联免疫分析法对瘦素和脂联素进行检测。用放射免疫法(RIA)对胰岛素进行检测。结果非酒精性脂肪肝患者的胰岛素及瘦素达显著升高(P<0.01),较正常对照组有显著性差异(P<0.01),且与脂肪肝病情的进程呈正相关,胰岛素抵抗与病程成正相关;而脂联素明显降低(P<0.01),较正常对照组有显著性差异(P<0.01),且与病情的进程呈负相关。结论胰岛素抵抗(IR)和脂质代谢紊乱导致的肝细胞脂质沉积,加重脂肪肝的进程,高瘦素浓度可致血胰岛素水平上升及肝细胞胰岛素抵抗,改变信号转导,加重脂酸堆积从而促进脂肪肝发生。
Objective To investigate the role of insulin, such as Insulin, leptin and Adiponectin, in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Methods 141 cases of non-alcoholic fatty liver were confirmed (42 cases of mild fatty liver, 51 cases of moderate fatty liver and 48 cases of severe fatty liver). Forty healthy people were selected as the control group. Leptin and adiponectin were detected by enzyme-linked immunosorbent assay. Insulin was tested by radioimmunoassay (RIA). Results The levels of insulin and leptin in patients with non-alcoholic fatty liver increased significantly (P <0.01), which were significantly different from those in normal control group (P <0.01), and were positively correlated with the progression of fatty liver disease. Insulin resistance and duration (P <0.01), which was significantly lower than that of the normal control group (P <0.01), and negatively correlated with the progression of the disease. Conclusions Insulin resistance (IR) and lipid metabolism disorders lead to lipid deposition in hepatocytes, which aggravates the progression of fatty liver. High leptin concentration can lead to the increase of blood insulin and hepatocyte insulin resistance, which can change the signal transduction and increase the accumulation of fatty acid Fatty liver occurs.