Alert date July 3, 2022

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FAT AS FUEL

The team embarked on the study based on observations that people with a high body-mass index and conditions like cardiovascular disease and diabetes are more sensitive to the disease.

The virus that causes COVID-19 undertakes a massive takeover of the body’s fat-processing system, creating cellular storehouses of fat that empower the virus to hijack the body’s molecular machinery and cause disease.

The team found that SARS-CoV2 doesn’t simply boost the number of triglycerides in our cells. The virus also changes much of our fat-processing system, changing the body’s ability to use fat as fuel.

THE SCIENCE RESEARCH SHOWED WEIGH LOSS DRUGS CAN STOP THE MASSIVE TAKEOVER OF YOUR FAT CELL MAKING SYSTEM.

After scientists discovered the important role of fat for SARS-CoV-2, they used weight-loss drugs and other fat-targeting compounds to try to stop the virus in cell culture. Cut off from its fatty fuel, the virus stopped replicating within 48 hours.

An approved weight-loss medication, Orlistat, a lipase inhibitor, stopped viral replication. An experimental compound known as GSK2194069 also stopped the virus. These and other compounds worked against all the SARS-CoV2 variants tested: alpha, beta, gamma and delta.

The authors of the recent paper in Nature Communications caution that the results are in cell culture, not in people; much more research remains to see if such compounds hold promise for people diagnosed with COVID. But the scientists, from Oregon Health & Science University and the Department of Energy’s Pacific Northwest National Laboratory, call the work a significant step toward understanding the virus.