Classically, obesity is considered to be due to a surplus of energy
intake over energy expenditure, resulting in storage of excess energy
as a fat (Fig. 1A). Genetic, physiological, and environmental factors
(e.g., high fat diet [HFD] and sedentary lifestyle) also play a significant
role in the etiology of obesity and obesity-associated metabolic disorders.
An innovative concept that has been recently proposed involves
the gut–liver axis as a critical component of obesity and NAFLD pathogenesis.
The latest advances in the field suggest that the increased
consumption of obesogenic foods (particularly those enriched in fat
and fructose) may alter the gut microbiota and intestinal barrier
function favoring the occurrence of metabolic endotoxemia and lowgrade
inflammation [4,5], thereby contributing to the development of
obesity and obesity-associated fatty liver disease (Fig. 1B).