Abstract
Oxidative stress plays a pivotal role in non-alcoholic fatty liver disease (NAFLD). Factors inducing oxidative stress in NAFLD may be several; however, a relationship with the adherence to Mediterranean Diet (Med-diet) and with serum lipopolysaccharide (LPS) has been poorly investigated in this setting. The aim was to investigate factors associated with impaired oxidative stress in NAFLD, focusing on the potential role of LPS and Med-diet. We enrolled 238 consecutive outpatients from the PLINIO study, in whom we measured the soluble Nox2-derived peptide (sNox2-dp), a marker of systemic oxidative stress, and serum LPS. Adherence to Med-diet was investigated by a nine-item validated dietary questionnaire. Serum sNox2-dp and LPS were higher in patients with NAFLD compared to those without (25.0 vs. 9.0 pg/mL, p < 0.001 and 62.0 vs. 44.9 pg/mL, p < 0.001, respectively). In patients with NAFLD, the highest sNox2-dp tertile was associated with the top serum LPS tertile (Odds Ratio (OR): 4.71; p < 0.001), APRI > 0.7 (OR: 6.96; p = 0.005) and Med-diet-score > 6 (OR: 0.14; p = 0.026). Analyzing individual foods, the daily consumption of wine (OR: 0.29, p = 0.046) and the adequate weekly consumption of fish (OR: 0.32, p = 0.030) inversely correlated with the top sNox2-dp tertile. In conclusion, patients with NAFLD showed impaired oxidative stress. Levels of sNox2 correlated with serum LPS and with low adherence to Med-Diet.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide [1].The spread of NAFLD is strongly associated with the increasing prevalence of obesity and type 2 diabetes because of changing lifestyles and unhealthy dietary habits [2].Based on the so-called “multiple parallel hits hypothesis”, oxidative stress plays a pivotal role in NAFLD onset and progression from simple steatosis (NAFL) to steatohepatitis (NASH) [3].The increased production of reactive oxygen species (ROS) is known to cause lipid peroxidation, followed by inflammation, and activation of stellate cells leading to fibrogenesis [4]
Elevated serum sNox2-dp levels have been described in several chronic inflammatory and metabolic diseases, including NAFLD [6,7]
44.9 (31.8–58.0) pg/mL, p < 0.001) were significantly higher in patients with NAFLD in comparison to to patients without analysis, sNox2-dp correlated with Med-Diet patients without
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide [1].The spread of NAFLD is strongly associated with the increasing prevalence of obesity and type 2 diabetes because of changing lifestyles and unhealthy dietary habits [2].Based on the so-called “multiple parallel hits hypothesis”, oxidative stress plays a pivotal role in NAFLD onset and progression from simple steatosis (NAFL) to steatohepatitis (NASH) [3].The increased production of reactive oxygen species (ROS) is known to cause lipid peroxidation, followed by inflammation, and activation of stellate cells leading to fibrogenesis [4]. Based on the so-called “multiple parallel hits hypothesis”, oxidative stress plays a pivotal role in NAFLD onset and progression from simple steatosis (NAFL) to steatohepatitis (NASH) [3]. Soluble NADPH oxidase 2-derived peptide (sNox2-dp) is a marker of NADPH oxidase activation, which is a major source of extracellular ROS [5]. Elevated serum sNox2-dp levels have been described in several chronic inflammatory and metabolic diseases, including NAFLD [6,7]. We demonstrated increased markers of systemic oxidative stress in subjects with NAFLD. SNox2-dp levels were increased independently from obesity, diabetes and metabolic syndrome and correlated with the severity of liver steatosis at ultrasound [8]
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