COVID-19 and obesity: the meeting of two pandemics

Abstract

COVID-19 and obesity are two pandemic diseases that the world is currently facing. Both activate the immune system and mediate inflammation. A sequence of disease phases in patients with severe COVID-19 results in a cytokine storm, which amplifies the subclinical inflammation that already exists in patients with obesity. Pro-inflammatory cytokines and chemotactic factors increase insulin resistance in obesity. Therefore, a greater systemic inflammatory response is establishe, along with an increased risk of thrombotic phenomena and hyperglycemic conditions. These changes further impair pulmonary, cardiac, hepatic, and renal functions, in addition to hindering glycemic control in people with diabetes and pre-diabetes. This review explains the pathophysiological mechanisms of these two pandemic diseases, provides a deeper understanding of this harmful interaction and lists possible therapeutic strategies for this risk group.

Keywords: COVID-19; inflammation; insulin resistance; obesity; pandemics.

Figure 1. Coronavirus replication cycle. : Created by BioRender.com

Figure 2. Deregulation of the renin-angiotensin-aldosterone system in COVID-19. : The justaglomerular cells of the afferent arterioles of the nephrons release renin which will convert angiotensinogen into angiotensin I. Then, this molecule is converted into angiotensin II (Ang II) through the action of the angiotensin-converting enzyme 1 (ACE), which is complex with its AT1 receptor (AT1R), leading to a pro-inflammatory, pro-oxidative and pro-fibrotic environment. ACE2 converts angiotensin I and Ang II to Ang 1-7, which produces contrary effects to Ang II when it binds to the Mas receptor (MAS R). A reduction or inhibition of ACE2 is observed in COVID-19 due to the binding of SARS-CoV-2 on the cell surface, leading to more severe pro-inflammatory reactions and more extensive tissue damage. : Adapted with permission from Brandão SCS and cols. (1,31). Created with Biorender.com.