Obesity and NAFLD: Same Problem?

Abstract

Obesity—namely visceral obesity—is definitely the core of the metabolic syndrome, having insulin resistance as the central metabolic defect. Body fat accumulation and insulin resistance mutually feed each other, and progressive lipotoxicity, i.e., accumulation of fat in adipose tissue stores, finally involves several organs, including the liver. The primary defect may be genetic in origin, or promoted by epigenetic modifications, or, more commonly, by unhealthy lifestyles (both unhealthy diet and poor physical activity), progressively leading to obesity. Nonalcoholic fatty liver disease is one of such conditions, possibly further impairing insulin sensitivity and favoring other comorbidities. The presence of “lean NAFLD” does not confute this theory: it must be regarded as a condition with a much more genetic imprinting in subjects who long maintain an adequate lifestyle. However, in most cases, favored by the accumulation of body fat and reduced physical activity that are common along the years, also these subjects are prone to develop visceral obesity. They might be considered “metabolically unhealthy normal weight” subjects, as opposed to the “metabolically healthy obese” individuals. In most cases, a variable drive of genes and lifestyle is probably the basis for differences that tend to produce obesity and metabolic diseases, including NAFLD, in the course of life.