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Introduction
Nonalcoholic fatty liver disease (NAFLD) is a liver disorder that is histologically similar to alcoholic fatty liver disease but occurs in patients who do not consume alcohol or with consumption limit of >30 g/day in men and >20 g/day in women (Riani et al., 2017; Chalasani et al., 2012). NAFLD is caused by an abnormality in fat metabolism resulting in the accumulation of fat in the liver cells (Riani et al., 2017). Several studies have shown that NAFLD and non-alcoholic steato hepatitis (NASH) prevalence rates have risen from 17% to 33% for NAFLD and 5.7% to 17% for NASH. The amount of fatty liver patients has increased year by year at Dr Kariadi Hospital Semarang (Purnomo et al., 2018). In a subgroup of patients, the inflammatory response of adipose tissue results in the release of several proinflammatory and profibrotic cytokines, which together with steatosis induce oxidative stress and activate fibrogenic hepatic stellate cells to cause NASH, hepatic fibrosis and cirrhosis (Smith and Adams, 2011).
The relation between visceral fat, oxidative stress and resistance to insulin has attracted attention. It was unclear or incomplete to explain this connection, mostly focusing on an individual detail of a specific pathway or pathogenesis (Purnomo et al., 2018). High visceral fat deposition is one of the risk factors for the incidence of severe NAFLD (Riani et al., 2017). In obesity, the deposition of visceral fat will result in the expansion of adipose tissues, which becomes a site for the accumulation of tumor necrosis factor-α stimulates proinflammatory cytokines, causing inflammatory reaction and fibrosis. In addition, Kupffer cells are activated to produce C-reactive proteins and prothrombotic molecules, resulting in the oxidation of fatty acids in the liver cells, which are the source reactive oxygen species (ROS), and then liver tissue damage as described in the second event of the two-hit hypothesis (Zivkovic et al., 2007). NAFLD is strongly associated with insulin resistance (IR) in the liver and adipose tissue and reduced insulin sensitivity throughout the body (Utzschneider and Kahn, 2006). IR is not only involved in hepatic steatosis but also in the development of oxidative stress by reducing mitochondrial beta oxidation leading to the activation of other oxidation pathways, thereby contributing to increased ROS level (Leach