Department of Community Nutrition, Faculty of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Epidemiology and Biostatistics, Faculty of Public Health, Zabol University of Medical Sciences, Zabol, Iran.
Eur J Clin Invest. 2020 Apr;50(4):e13211. doi: 10.1111/eci.13211. Epub 2020 Feb 25.
Oxidative stress is one of the major pathologic mechanisms for the progression of nonalcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the relationship between the extent of steatosis and oxidative stress parameters in patients with NAFLD.
The data obtained from 122 patients with NAFLD and 106 healthy controls aged 20-60 years with body mass index (BMI) ranging from 25 to 35 kg/m . Abdominal ultrasonography was performed in participants in order to the grading of hepatic steatosis. Fasting blood samples and anthropometric measurements were collected for all study subjects. Oxidative stress was evaluated by measurement of serum malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), total antioxidant capacity (TAC) and erythrocyte superoxide dismutase (SOD) as well as glutathione peroxidase (GPx) activities.
Serum levels of liver enzymes (P < .0001) and MDA (P = .018), as well as erythrocyte SOD activity (P < .0001), were significantly higher in patients with NAFLD compared to healthy controls. Furthermore, patients with NAFLD had significantly lower serum TAC levels compared to healthy controls (P < .0001). No significant differences were observed in serum ox-LDL level and erythrocyte GPx activity between the groups. The probability of being NAFLD increased with increasing serum levels of MDA (P = .020) and SOD activity (P < .0001). In contrast, decreased serum TAC levels predicted the probability of being NAFLD (P < .0001).
Increased extent of hepatic steatosis could be considered as a pathological mechanism for enhancing oxidative stress in patients with NAFLD, independent of obesity, and is exacerbated further in patients with more severe condition.
氧化应激是非酒精性脂肪性肝病(NAFLD)进展的主要病理机制之一。本研究旨在评估 NAFLD 患者脂肪变性程度与氧化应激参数之间的关系。
对 122 名年龄在 20-60 岁、体重指数(BMI)在 25-35 kg/m 之间的 NAFLD 患者和 106 名健康对照者进行了数据分析,以评估肝脏脂肪变性程度。所有研究对象均采集空腹血样和人体测量学数据。通过测量血清丙二醛(MDA)、氧化型低密度脂蛋白(ox-LDL)、总抗氧化能力(TAC)和红细胞超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GPx)活性来评估氧化应激。
与健康对照组相比,NAFLD 患者的血清肝酶水平(P <.0001)、MDA 水平(P =.018)和红细胞 SOD 活性(P <.0001)显著升高,而 TAC 水平显著降低(P <.0001)。两组间血清 ox-LDL 水平和红细胞 GPx 活性无显著差异。MDA 水平(P =.020)和 SOD 活性(P <.0001)升高与 NAFLD 发生的概率增加有关。相反,血清 TAC 水平降低预示着 NAFLD 发生的概率增加(P <.0001)。
肝脏脂肪变性程度的增加可被视为 NAFLD 患者氧化应激增强的病理机制,这种情况独立于肥胖,且在病情更严重的患者中进一步恶化。