Fig. 2.

Obesity, co-morbidities and COVID-19 (coronavirus disease 2019): the triple burden. Obesity and its co-morbidities induce low-grade chronic inflammation and an increase in angiotensin-converting enzyme 2 (ACE2) receptors present in the lungs, intestine and kidneys. COVID-19, in turn, also induces inflammation and alterations overlapping those induced by obesity and its co-morbidities. These alterations occur as the disease severity increases and are in: glycaemia – increasing blood glucose; the renin–angiotensin system – causing higher pro-inflammatory responses; lung function – increasing vascular permeability and lung injury; the coagulation system – increasing prothrombotic effects; kidney function – inducing chronic kidney failure. Possible pathways to explain these worsened alterations in patients with obesity and with co-morbidities are: in the lungs – a higher ACE2 expression, unregulated lipogenesis and inflammation; in the coagulation system – a higher concentration of plasminogen activator inhibitor-1; and in the kidney – a higher expression of ACE2 and transmembrane protease serine (TMPRSS) genes. These overlapping alterations and inflammation associated with the cytokine storm induced by COVID-19 increase the risk of complications in patients with obesity, such as respiratory failure, septic shock, multiple organ failure, and, ultimately, increased mortality.