Evaluating Possible Mechanisms Linking Obesity to COVID-19: a Narrative Review

Abstract

Currently, pneumonia caused by the coronavirus disease 2019 (COVID-19) is a pandemic. To date, there is no specific antiviral treatment for the disease, and universal access to the vaccine is a serious challenge. Some observational studies have shown that COVID-19 is more common in countries with a high prevalence of obesity and that people with COVID-19 have a higher body mass index. In these studies, obesity increased the risk of disease, as well as its severity and mortality. This study aimed to review the mechanisms that link obesity to COVID-19.

Keywords: Adipokines; COVID-19; Cardiovascular system; Inflammation; Insulin resistance; Obesity; Respiratory; SARS-CoV-2; Thromboembolism.

Fig. 1

Possible pathways linking obesity to COVID-19

Fig. 2

The function of the immune system when a SARS-CoV-2 virus enters the body. Several cytokines and adipokines are released by the vascular endothelium, adipose tissue, and T cells after exposure to the virus. Inappropriate activation of the immune system results in cytokine storm and hypercoagulability state. These conditions complicated the COVID-19 disease course and its management. Abbreviations: VCAM-1, vascular cell adhesion protein 1; MCP-1, monocyte chemoattractant protein-1; NOS, nitric oxide synthase; IL, interleukin; TNF-α, tumor necrosis factor alpha; TLR, toll-like receptor; ACE2, angiotensin-converting enzyme 2; DDP4, dipeptidyl peptidase-4; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells; STAT3, signal transducer and activator of transcription 3; MQ, macrophage cell; NK cell, natural killer cell; IFN-γ, interferon-gamma; Th, T helper cell; CCL-2, chemokine (C–C motif) ligand 2; IG, immunoglobulin