Research suggests GLP-1 receptor agonist drugs may help prevent pulmonary fibrosis in people with type 2 diabetes who develop long COVID.
- People with type 2 diabetes have four times higher risk of developing pulmonary fibrosis after COVID-19 infection compared to those without diabetes
- Study found that GLP-1s regulated fibrosis-related genes and reduced lung scarring in infected mouse models
According to research published in the Journal of Virology, there may be a new, nonglycemic application for glucagon-like peptide-1 receptor agonists (GLP-1 RAs). The research suggests the drugs could help prevent pulmonary fibrosis in people who have type 2 diabetes (TD2) and long COVID.
The research results are detailed in the paper, “Glucagon-Like Peptide-1 Receptor Agonist Prevents Pulmonary Fibrosis Following Acute COVID-19 Infection Associated With Type 2 Diabetes.”
Anyone who becomes infected with SARS-CoV-2, the virus that causes COVID-19, can develop health problems associated with long COVID, including pulmonary fibrosis. However, studies estimate that this risk is four times higher in people with TD2 than those without.
“People with diabetes have way more severe infections and infection-related severe disease after COVID-19 than other people. We wanted to know why these people have long-term symptoms,” said lead investigator Runhong Zhou, PhD, a virologist at the University of Hong Kong, in a press release.
To begin the study, Dr. Zhou and team analyzed a previously published dataset of blood samples from individuals who were hospitalized for COVID-19 treatment. They compared patients with diabetes (n=11) and without (n=79) at three specific intervals: hospital admission, five days postadmission and two to three months postadmission. At the third follow-up period, people with diabetes showed increased levels of monocytes, including cathepsin D, HIF-1α and lactate dehydrogenase A, that are associated with pulmonary fibrosis.
The researchers tested these findings on mouse models and confirmed that several fibrosis-related genes were overly active in the infected mice.
“Long COVID is a continuous issue, and especially a lot of elderly people are still suffering from this. So, to find a solution to help these patients is an important issue,” said Zhiwei Chen, PhD, who is also a virologist at the University of Hong Kong.
The research team decided to try treating the infected mice with an in-house GLP-1 RA. Dr. Zhou said he knew the GLP-1 receptor is highly expressed in lung cells and he had read other studies of GLP-1 RAs providing anti-inflammatory benefits against fibrosis, but he had not seen experiments testing the effects in animal models in relation to long COVID.
The results were positive: The GLP-1 RA appeared to regulate the fibrosis-related genes and reprogram the macrophages that can cause a buildup of scar tissue in the lungs. The treated mice had less pulmonary fibrosis than those not treated with the drug, the authors reported.
Dr. Zhou said their research is preliminary, showing only proof of concept, but is worth further investigation.
