 |
|
|
| |
SARS-CoV-2 Rewires Lipid and Metabolic Profiles, Posing Heart and Liver Risks
|
| |
| |
AASLD The Liver Meeting Digital Experience, November 13-16, 2020
Mark Mascolini
SARS-CoV-2, the virus that causes COVID-19, had profound impacts of lipid and metabolic profiles in infected people, according to a study using nuclear magnetic resonance (NMR)-based technology [1]. Changes associated with SARS-CoV-2, say researchers from CIC bioGUNE in Spain, could heighten the risk of atherogenic and liver disease in people with COVID-19.
Everyone now recognizes that COVID-19 affects not only the lungs, but other major organs and systems as well. The list already includes the liver, kidneys, cardiovascular and central nervous systems, the gastrointestinal tract, and blood. Researchers from the Precision Medicine and Metabolism Lab of CIC bioGUNE in Spain use NMR to analyze metabolomics and lipidomics and their impact on multisystem disease.
They conducted this study to analyze the metabolic and lipid profiles of people diagnosed with COVID-19 by PCR detection of SARS-CoV-2. Using NMR-based metabolomics, they assessed three serum cohorts: (1) COVIDpos: 400 COVID-19-positive samples from people with SARS-CoV-2 infection and pneumonia, (2) COVIDneg: 60 samples from people with pneumonia but negative for SARS-CoV-2, and (3) preCOVID: 280 samples from healthy individuals collected before the COVID-19 pandemic.
Serum profiling showed two potentially important changes: (1) significantly higher levels of the inflammation marker GlycA in the COVIDpos group than in the COVIDneg or preCOVID group, and (2) accumulation of porphyrins in COVIDpos samples, specifically uroporphyrin I and coproporphyrin I. Porphyrin accumulation may explain some COVID-19 symptoms, the researcher suggested, similar to those of the liver disorders called porphyria.
Lipidomic analysis uncovered a "clear pathogenic redistribution" of lipoprotein particle size and composition in the COVIDpos cohort compared with normal preCOVID samples. The researchers charted reduced HDL size, enlarged LDL size, and higher levels of VLDL subclasses with intermediate sizes. The Apo-B to Apo-A1 ratio increased markedly in COVIDpos samples, upsetting the balance between atherogenic and antiatherogenic particles. These lipid changes all point to heightened cardiovascular risk in people with COVID-19.
Metabolomic profiling revealed several changes: Among amino acids, levels of phenylalanine and glutamic acid rose, while levels of methionine, isoleucine, lysine, and others fell. The profiling also tracked increases in glucose, ketone bodies, carboxylic acids, and organic acids. These changes could reflect liver damage, the researchers suggested, via dysregulation of hepatic central metabolism, oxidative stress, and mitochondrial
dysfunction.
Summarizing this largest metabolomic study of serum samples from people with COVID-19, the researchers concluded that "SARS-CoV-2 infection dysregulates-or "rewires"-the metabolomic and lipidomic profiles of serum and induces dramatic changes in liver metabolism and blood composition." These changes, they added, "are consistent with the severe phenotype found in COVID-19 patients . . . and highlight the systemic nature of the disease."
Reference
1. Bruzzone C, Bizkarguenaga M, GilRedondo R, et al. SARS-CoV-2 infection produces serum porphyrin accumulation, dyslipidemia and severe metabolic dysregulation. AASLD The Liver Meeting Digital Experience, November 13-16, 2020. Abstract 105.
|
| |
|
|
|
|
|
