Table 1.
Reference | Study design | Co-morbidity associated with obesity | Relationship with the worsening prognostic of coronavirus infections |
---|---|---|---|
Yang et al.(164) | Human study, retrospective analysis | Hyperglycaemia and hypertension | Patients admitted to Beijing hospitals diagnosed with SARS showed increased risk of severe hypoxia and death risk, due to hyperglycaemia and ketosis effects |
Kulcsar et al.(105) | Mouse model | Type 2 diabetes | Mice with diabetes showed increased expression of IL-17a after infection by MERS-CoV |
Al Heialy et al.(98) | Re-analysis of publicly available transcriptomic data and mouse model | Diabetes | Human pulmonary epithelial cells infected with SARS-CoV-2 presented positive regulation of the suppressor of the SOC3 gene, which regulates inflammation and inhibits leptin signalling, favouring viral replication. A mouse model of diet-induced obesity showed increased ACE2 expression in the lungs by the suppression of genes that encode SREBP1 |
Zheng et al.(118) | Human case–control study | MAFLD | A multi-centre study involving 214 patients with laboratory-confirmed COVID-19 aged between 18 and 75 years of three hospitals in the city of Wenzhou (China) to investigate the association between MAFLD and COVID-19 severity. Data showed that the presence of obesity in patients with MAFLD increased six-fold the risk for severe COVID-19 |
SARS, severe acute respiratory syndrome; MERS-CoV, Middle East respiratory syndrome coronavirus; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SOC3, suppressor of cytokine signalling 3; ACE2, angiotensin-converting enzyme 2; SREBP1, sterol regulatory element-binding protein 1; MAFLD, metabolic associated fatty liver disease; COVID-19, coronavirus disease 2019.