Adipose tissue dysfunction and MAFLD in obesity on the scene of COVID-19.

Obesity is a known risk factor for respiratory infection and many other chronic diseases, including metabolic dysfunction-associated fatty liver disease (MAFLD), previously known as nonalcoholic fatty liver disease (NAFLD). Recently, it has been considered an important and independent predictor for coronavirus disease 2019 (COVID-19) complications in adults, especially cardiopulmonary, presenting in a great number of individuals in critical care. In obesity, adipose tissue (AT) undergoes expansion via several processes: expansion of adipocytes and insufficient vascularization lead to hypoxia; adipocyte apoptosis/necrosis; irregular fatty acid flux; and enhanced secretion of inflammatory adipokines, cytokines, and chemokines. In individuals with obesity the liver can also become a target of COVID-19 infection, although major liver damage is uncommon. COVID-19 acute pandemic often develops in patients with major metabolic abnormalities, including fatty liver disease, which is part of a chronic pandemic together with body fat accumulation. During metabolic abnormalities, the expansion of metabolically active fat parallels chronic inflammatory changes, the development of Insulin Resistance (IR), and in the liver, the accumulation of fat, possibly, an underlying fibrosis. SARS-Cov-2 virus might affect the liver by direct or indirect mechanisms. The current epidemic of obesity and related metabolic diseases has extensively contributed to increase the number of severe cases and deaths from COVID-19, resulting in a health, political and economic crisis with long-lasting consequences. In this review, the authors explore the relationship between AT dysfunction and MAFLD in obesity on the scene of COVID-19.