The surprising link between SARS-CoV-2 infection and new-onset diabetes

Pathogenesis and treatment strategies for COVID-19 symptoms. The insulin/IGF pathway plays an important part in many biological processes such as energy metabolism, cell survival, and cell growth. SARS-CoV-2 causes a decrease in transcription of the insulin/IGF pathway in the host lung and liver adipose tissues. The pathological trait is aggravated by whole blood in critical patients with COVID-19. This is likely due to interferon regulatory factor 1 (IRF1). Higher basal IRF1 levels may be due to pathological factors (older age and male sex, obesity and diabetes), and could result in synergistic upregulations of IRF1 in response SARS-CoV-2 infections. This could make people more susceptible to COVID-19. Credit: Osaka University. CC BY

It is now clear that coronavirus virus 19 (COVID-19) can cause serious complications beyond the lungs. Japanese researchers have now identified the key gene that controls the effects of SARS-2 virus infection on blood sugar metabolism.

In a June study, MetabolismResearchers at Osaka University discovered that COVID-19 interferes with insulin signaling and can cause metabolic problems and even diabetes.

COVID-19 is most well-known for causing respiratory diseases, but it can also cause damage to other organ systems. For example, disruptions in blood sugar regulation could lead to new-onset diabetes. It is not clear how the SARS-CoV-2 virus causes these effects.

Jihoon Shin (first author of the study) says that the insulin/IGF signaling pathway plays a crucial role in cell survival and energy metabolism. “We suspected that SARS/CoV-2 could affect this signaling pathway and cause problems with blood sugar regulation,” says Jihoon Shin, first author of the study.

The researchers used data from patients and models in vivo and vitro infected by SARS-CoV-2 to test this hypothesis. They looked for genes that were significantly over- or under-expressed in comparison to uninfected animals, cells, or patients.

Iichiro Shimomura (senior author of the study) stated that “the results were striking.” “Infection with SARS-2 caused changes in insulin/IGF signaling pathway components of the liver, pancreatic, and lung. These changes could also be attributed to activation IRF1 (interferon regulator factor 1).

Further investigation revealed that IRF1 is expressed in higher numbers in older patients, patients with diabetes, obese people, and patients with obesity. Due to the synergistic effects of older age, male sexual activity, obesity, and diabetes with SARS-2, IRF1 expression is higher in these patients, which may explain their vulnerability to COVID-19. Critical patients with COVID-19 had higher IRF1 levels and lower insulin/IGF signaling pathway gene expression than noncritical patients. Finally, treating SARS-CoV-2–infected cells or an animal model with hormonal factors that decreased IRF1 expression enhanced insulin/IGF signaling.

“Our findings show that SARS/CoV-2 infection impairs insulin/IGF signals by increasing IRF1 transcription, which in turn disrupts blood sugar metabolism. Shin suggests that treatment with factors such dihydrotestosterone, dexamethasone and IRF1 could decrease IRF1 expression to help reduce the effects of COVID-19.

COVID-19 can have a devastating effect on multiple organ systems. Therefore, it is important to develop treatment strategies that reduce the disease’s impact on blood sugar metabolism. Some of the severe effects of COVID-19 can be avoided by identifying those at higher risk and intervening to reduce IRF1 activation.

Your risk of developing COVID-19 could be reduced by lowering your blood insulin levels

More information:
Jihoon Shin and colleagues, SARS-CoV-2 infected pancreatic cells, liver, and lung with IRF1 impairs insulin/IGF signaling pathways. Metabolism (2022). DOI: 10.1016/j.metabol.2022.155236

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Osaka University

Surprising connection between SARS/CoV-2 infection (2022, June 27)
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