SARS-CoV-2-infected adipocytes drive adipose inflammation and hepatocyte lipid accumulation.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Obesity and fatty liver may worsen COVID-19 outcomes, but the mechanism by which adipose tissue infection contributes to liver injury is unclear. We aimed to determine whether SARS-CoV-2 infection of human adipocytes promotes inflammation and hepatic lipid accumulation, and to identify the underlying mechanisms. Mesenchymal stem cell-derived human adipocytes were infected with Wuhan SARS-CoV-2 strain. Cell-surface ACE2 expression was measured in adipocytes. Viral replication and infectious titers were measured, and adipocyte morphology, cytokine/adipokine secretion, and lipid metabolism gene expression were analyzed. Culture supernatants from infected adipocytes were then applied to Huh7.5 hepatocytes to evaluate steatosis and fibrogenic activation. SARS-CoV-2 productively infected adipocytes, which express cell-surface ACE2, leading to hypertrophy, increased IL-6 secretion, a higher leptin/adiponectin ratio, and lipid droplet accumulation. The infectious virus was released into the supernatants. However, neutralization with anti-Spike antibodies or UV-C inactivation abolished this effect, indicating that hepatocyte lipid accumulation depended on infectious virus rather than on soluble adipocyte-derived mediators alone. Adipose tissue can serve as a source of infectious SARS-CoV-2 that promotes hepatic steatosis and fibrogenic activation, suggesting a mechanism by which obesity

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.