Research evidence suggests that adipocytes in obesity might facilitate SARS-CoV-2 replication, for it was only found in adipose tissue of individuals with overweight or obesity but not lean individuals who died from COVID-19. As lipid metabolism is key to adipocyte function, and viruses are capable of exploiting and manipulating lipid metabolism of host cells for their own benefit of infection, we hypothesize that adipocytes could not only impair host immune defense against viral infection, but also facilitate SARS-CoV-2 entry, replication and assembly as a reservoir to boost the viral infection in obesity. The latter of which could mainly be mediated by SARS-CoV-2 hijacking the abnormal lipid metabolism in the adipocytes. If these were to be confirmed, an approach to combat COVID-19 in people with obesity by taking advantage of the abnormal lipid metabolism in adipocytes might be considered, as well as modifying lipid metabolism of other host cells as a potential adjunctive treatment for COVID-19.
Keywords: ACE2, angiotensin-converting enzyme 2; ATP, adenosine triphosphate; Adipocyte; COVID-19, coronavirus disease 2019; ER, endoplasmic reticulum; ERGIC, ER-to-Golgi intermediate compartment; FFAs, free fatty acids; LDs, lipid droplets; Lipid metabolism; Obesity; S protein, spike protein; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; Severe acute respiratory syndrome coronavirus 2; TAGs, triacylglycerols.
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