The HCCDB gene expression database (http://lifeome.net/database/hccdb/home.html) was used to determine ACE2 expression levels in both human adipose and lung tissue.  

- ACE2 gene expression was higher in both subcutaneous and visceral adipose tissue compared to lung tissue
- previous studies have shown that obesity alone does not affect ACE2 expression, but this study shows that obese individuals with more adipose tissue will consequently have more ACE2 receptors
- this study does not prove that SARS-CoV-2 can infect human adipose tissue or propose a possible mechanism of infection

ACE2 Expression in Adipose Tissue May Contribute to COVID-19 Morbidity and Mortality in Obese Patients

Ang II is a hormone that is regulated by the RAS.  The excessive adipose tissue associated with obesity is known to secrete this molecule which stimulates inflammation, insulin resistance, oxidative stress, and vasoconstriction.  Insulin resistance can exacerbate these conditions by further stimulating the RAS.  A relationship exists between pancreatic beta islet cells (B-cells) and the RAS: B-cell dysfunction leads to increased expression AT1R, the receptor for Ang II, and insulin resistance while RAS inhibition increases B-cell function and insulin sensitivity.  

Renin-Angiotensin System (RAS) Activity May Contribute to COVID-19 Morbidity and Mortality in Obese Patients

Endothelial dysfunction is associated with obesity and has been shown to lead to inflammation, oxidative stress, and vascular endothelial cell apoptosis.  These conditions may contribute to cytokine storm syndrome which is known to exacerbate COVID-19.  Additionally, the chronic inflammation and impaired ability to break down blood clots caused by endothelial dysfunction may lead to thrombosis, a condition that is thought to be mechanistically involved in severe lung damage and death in SARS-CoV-2 infections.  

Endothelial Dysfunction May Contribute to COVID-19 Morbidity and Mortality in Obese Patients

Cytokine storm occurs when the immune system over-responds.  Obesity is associated with increased inflammation, especially in liver and visceral adipose tissue.  Pro-inflammatory adipokines and cytokines can be produced by adipose tissue, have the ability to weaken an immune response, and have been linked to decreased pulmonary function.  An associative study showed that interlukin-6 (IL-6) levels are increased in these tissues in obesity which may prompt a more severe case of COVID-19 upon SARS-CoV-2 infection.  

Cytokine Storm as a Risk Factor for Obese Patient Morbidity/Mortality in COVID-19

- ACE2 expression
- RAS activity
- cytokine storm
- endothelial dysfunction

Michigan State University

- Risk of infection
- Effects by geographical location
- Proposed disease mechanisms that contribute to morbidity and mortality
- COVID-19 complications and outcomes

Focuses of Obesity in COVID-19 Patients

- China
- Italy
- Spain
- United States
- France
- United Kingdom
- Mexico

Obesity in COVID-19 Patients by Geographic Location

Proposed Mechanisms Related to Obesity that Contribute to COVID-19 Morbidity and Mortality

- In-hospital mortality 
- Risk of intubation 
- Acute kidney injury 
- Acute respiratory distress syndrome 
- Acute cardiac injury 

Effects of Obesity on COVID-19 Complications and Outcomes 

Researchers have found individuals with body fat higher or lower than normal had a higher risk of disease infection. 

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