Targher G, Bertolini L, Scala L, Zoppini G, Zenari L, Falezza G
Department of Internal Medicine, Sacro Cuore Hospital of Negrar (VR), Verona, Italy.
Diabet Med. 2005 Oct;22(10):1354-8. doi: 10.1111/j.1464-5491.2005.01646.x.
To compare plasma biomarkers of inflammation and endothelial dysfunction in individuals with and without non-alcoholic hepatic steatosis (HS), and to evaluate whether such differences were mediated by the adverse metabolic pattern, typically found in these subjects.
HS (by ultrasound and computed tomography), visceral fat (by computed tomography), insulin resistance (by homeostasis model assessment-HOMA), plasma biomarkers of inflammation and endothelial dysfunction (hs-C reactive protein, fibrinogen, von Willebrand factor, plasminogen activator inhibitor-1 activity) were measured in 100 non-smoking, healthy, male volunteers.
Plasma hs-CRP, fibrinogen, v-WF and plasminogen activator inhibitor-1 (PAI-1) activity levels were markedly higher (P < 0.01 or less) in subjects with non-alcoholic HS (n = 35) than in those without HS (n = 65). The former also had significantly higher values for body mass index (BMI), visceral fat, diastolic blood pressure, HOMA insulin resistance score, plasma insulin (both fasting and after glucose load), triglycerides, liver enzymes, and lower high-density lipoprotein (HDL)-cholesterol concentration. While the marked differences in these pro-inflammatory biomarkers observed between the groups were little affected by adjustment for age, BMI, blood pressure values, HOMA insulin resistance score, plasma triglyceride and liver enzyme concentrations, they were completely abolished after controlling for visceral fat. Similarly, in multivariate regression analyses, increased visceral fat significantly predicted the pro-inflammatory biomarkers, independently of HS and other potential confounders.
These results indicate that, in non-smoking, non-diabetic men, the significant increase of plasma biomarkers of inflammation and endothelial dysfunction in the presence of non-alcoholic HS is largely mediated by abdominal visceral fat accumulation.
比较有无非酒精性肝脂肪变性（HS）个体的炎症和内皮功能障碍血浆生物标志物，并评估这些差异是否由这些受试者典型的不良代谢模式介导。
对100名不吸烟、健康的男性志愿者测量HS（通过超声和计算机断层扫描）、内脏脂肪（通过计算机断层扫描）、胰岛素抵抗（通过稳态模型评估-HOMA）、炎症和内皮功能障碍血浆生物标志物（高敏C反应蛋白、纤维蛋白原、血管性血友病因子、纤溶酶原激活物抑制剂-1活性）。
非酒精性HS患者（n = 35）的血浆高敏CRP、纤维蛋白原、血管性血友病因子和纤溶酶原激活物抑制剂-1（PAI-1）活性水平显著高于无HS患者（n = 65）（P < 0.01或更低）。前者的体重指数（BMI）、内脏脂肪、舒张压、HOMA胰岛素抵抗评分、血浆胰岛素（空腹和葡萄糖负荷后）、甘油三酯、肝酶也显著更高，而高密度脂蛋白（HDL）胆固醇浓度更低。虽然两组间观察到的这些促炎生物标志物的显著差异在调整年龄、BMI、血压值、HOMA胰岛素抵抗评分、血浆甘油三酯和肝酶浓度后受影响较小，但在控制内脏脂肪后差异完全消除。同样，在多变量回归分析中，内脏脂肪增加显著预测促炎生物标志物，独立于HS和其他潜在混杂因素。
这些结果表明，在不吸烟、非糖尿病男性中，非酒精性HS存在时炎症和内皮功能障碍血浆生物标志物的显著增加很大程度上由腹部内脏脂肪堆积介导。
