ABSTRACT
Ippokration Hospital, 49 Konstantinoupoleos Street, Thessaloniki 54124, Greece
Nonalcoholic fatty liver disease (NAFLD) has become the commonest form of liver disease in developed countries, aff ecting 20-30% of the general population. Th e pathogenesis is thought to be a multiple-hit process involving insulin resistance (IR), oxidative stress, apoptosis and adipokines. Adipose tissue has recently emerged as an active endocrine organ producing multiple proteins collectively referred to as adipokines. Th e release of adipokines plays an essential role in the pathogenesis of IR syndrome, including NAFLD, because they alter insulin sensitivity in insulin-targeted organs, such as the skeletal muscle and the liver. Some adipokines, including adiponectin, visfatin and acylation-stimulating protein, may positively infl uence insulin sensitivity, whereas others, including tumor necrosis factor α, interleukin 6 and resistin, infl uence insulin sensitivity negatively. Furthermore, classical cytokines, produced by immune cells infi ltrating adipose tissue, are involved in liver infl ammation and play an important role in the pathogenesis of NAFLD. Th e dynamic balance and interactions among various adipokines/cytokines, which improve or worsen IR, lead to the fi nal benefi cial or detrimental eff ect on NAFLD.
