ABSTRACT
Calorie-rich diets; consumption of energy-dense, high-fat, and/or high-sugar foods (sometimes called junk food) and beverages; and a lack of physical exercise, all habits that lead to obesity and are typical of the so-called civilized countries, have generated an explosion of hepatic steatosis or unclassied nonalcoholic fatty liver disease (NAFLD), which can evolve into nonalcoholic steatohepatitis (NASH) or, simply, fatty liver. Increased production of adipokines by adipose tissue and raised circulating levels of acute-phase proteins and inammatory cytokines have led to the view that obese people are characterized by a state of low-grade chronic inammation, causally linked to insulin resistance (IR) and the metabolic syndrome (MetSyn) [1]. In adult obese subjects, serum concentrations of C-reactive protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) have been signi- cantly correlated with body mass index (BMI) and waist circumference [2]. Low-grade systemic inammation also may underlie the clustering of metabolic risk factors in children and adolescents [3-6]. Through proteomics and microarray screening, Zhang et al. [7] identied lipocalin 2, a novel autocrine and paracrine adipokine that potentially links obesity with its related adipose inammation. In contrast, data from Wistar rats suggest that diet-induced obesity affects intracellular insulin signaling mechanisms leading to hepatic IR, which plays a determinant role in inducing NAFLD independently of the inammatory action of cytokines [8].
