Obesity and COVID-19: A jigsaw puzzle with still missing pieces

Abstract

Apart from posing various mechanical and medical issues compromising general health, obesity is a major factor for respiratory tract infections, due to specific inflammation and immunological compromise. The burden of obesity on morbidity and mortality of SARS-CoV-2 infection/COVID-19 is considerable. Herein, we aimed to search the literature and present to the readers pathophysiologic pathways that may associate obesity and COVID-19. We present potential mechanisms, which might partly explain why patients with obesity are more prone to suffer from respiratory infections in the context of COVID-19. Better understanding of these pathways could eventually guide management strategies and therapies for COVID-19 in the future.

FIGURE 1

A, Cytokines and inflammation in subjects with obesity. Release of inflammatory molecules represents the cornerstone of obesity‐induced inflammation. NF‐κB: Nuclear Factor kappa‐light chain‐enhancer of activated B‐cells. B, Adipose tissue and adipokines in subjects with obesity. Healthy adipose tissue secretes less leptin and more adiponectin, preventing inflammation. In obesity, this is inversed and reduced levels of the anti‐inflammatory adiponectin favour resistance to leptin and subsequent susceptibility to infections. This is notable for lung infections and critical illness that requires treatment in an intensive care unit (ICU). AGT, angiotensinogen; MCP‐1, monocyte chemoattractive protein‐1; PAI‐1, plasminogen activator inhibitor‐1; TGF‐β, transforming growth factor‐ β; VEGF, vascular endothelial growth factor