Should Physicians Consider NAFLD a Primary or Secondary Disease?

Dear Colleagues,

Obesity, dyslipidemia, hypertension, and type 2 diabetes mellitus (T2DM) are mostly prominent in Western societies (but are not restricted to these), and represent the well-known metabolic syndrome. Focusing on obesity, there is a great body of evidence that both genetic and environmental factors are important in its genesis and evolution. Whereas the genetic factors are still poorly understood, numerous studies have shown that particularly abdominal obesity and physical inactivity are central. Specifically, obesity is a major risk factor for the development of insulin resistance—a key factor in the etiology of the metabolic syndrome and T2DM. Obesity and insulin resistance promote the development of non-alcoholic fatty liver disease (NAFLD), which in a subset of patients can evolve in a more severe form (i.e., non-alcoholic steatohepatitis, NASH). NASH is characterized by fatty infiltration of the liver and inflammation leading to the apoptosis and necrosis of hepatocytes—features to which reparative responses follow, resulting in fibrosis. Unfortunately, research is far from completely clarifying the genesis of these diseases (NAFLD/NASH) and suggesting appropriate therapy to drastically reduce or eliminate them. Finally, there is still much debate as to whether NAFLD/NASH is a primary or secondary illness.

This Special Issue is set to gather research concerning the unknown mechanisms of these diseases and to confirm the consolidated ones with new observations.

Potential topics include but are not limited to the following:

• Obesity-related NAFLD;
• Non-obese NAFLD;
• Genetic NAFLD;
• Re-feeding NAFLD;
• PCOS-associated NAFLD;
• OSAS-associated NAFLD;
• Drug-induced NAFLD (including toxic substances);
• Juvenile NAFLD;
• Silent NASH;
• Is NAFLD really benign?
• The role of metabolic syndrome in the onset and worsening of NAFLD;
• The link between NAFLD and hepatocarcinoma;
• Immune system involvement, with special attention to the major immune organ (i.e., spleen);
• Chronic low-grade inflammation;
• Adipokines, hormones, and growth factors involved in the pathogenesis of NAFLD/NASH;
• Mitochondrial dysfunction at the basis of NAFLD;
• The interplay between microbiome and/or virome and NAFLD;
• Environmental factors linked to NAFLD;
• The emerging role of MUFAs.

Prof. Dr. Giovanni Tarantino
Guest Editor

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