Pathogenesis of COVID-19 symptoms and treatment strategies. The insulin / IGF signaling pathway plays an important role in many biological processes such as energy metabolism and cell survival. SARS-CoV-2 infection disrupts the transcriptional expression of the insulin / IGF signaling pathway in the host lung, adipose tissue of the liver, and pancreatic cells, possibly attributed to the regulatory factor interferon 1 (IRF1). The pathological trait is exacerbated in whole blood, a systemic indicator, of critical patients with COVID-19 with exacerbated cell damage, cell death, and metabolic abnormalities, which can be mediated by androgen (DHT) and / or glucocorticoid (DEX) interventions. Improve. Expression of higher basal IRF1 by pathological causes (older age, male, obesity, and diabetes) in respiratory, metabolic, and / or endocrine organs may help regulate IRF1 uptake and uptake in response to SARS-CoV-2 infection; This may make people more vulnerable to COVID-19. Credits: Osaka University, CC BY

It has been well established that coronavirus 19 (COVID-19) can have far-reaching detrimental effects beyond the lungs, despite being transmitted through the SARS-CoV-2 virus. Now, Japanese researchers have identified a gene that mediates the effects of SARS-CoV-2 infection on blood sugar metabolism.

In a study conducted in June metabolismResearchers at Osaka University have shown that COVID-19 can cause metabolic problems and sometimes even diabetes by interfering with insulin signaling.

COVID-19 is best known for causing respiratory diseases, but it can also damage other organ systems. In particular, dysregulation of blood sugar can lead to new diabetes. However, it is not clear how infection with the SARS-CoV-2 virus leads to these effects.

“The insulin / IGF signaling pathway is a key pathway in regulating energy metabolism and cell survival,” says Jeyhun Sheen, lead author of the study. Therefore, we suspected that SARS-CoV-2 affects this signaling pathway and causes problems in regulating blood sugar.

To test this, the researchers analyzed gene expression data from patients, as well as in vivo and in vitro models infected with SARS-CoV-2. In particular, they looked for genes that were significantly overexpressed or under-expressed compared to patients, animals, or non-infected cells.

“The results were amazing,” said Ichiro Shimomura, lead author of the study. “Infection with SARS-CoV-2 affects the expression of components of the insulin / IGF signaling pathway in the lung, liver, adipose tissue, and pancreatic cells. It is attributed. “

Further research has shown that IRF1 expression is increased in elderly patients, men, obese people and diabetics. The synergistic effect of older age, male gender, obesity and diabetes with SARS-CoV-2 means that IRF1 expression occurs more rapidly, which may explain why these patients are more vulnerable to COVID-19. In addition, critical patients with COVID-19 had higher IRF1 expression and lower insulin / IGF signaling genes in their blood than non-critical patients. Finally, treatment of SARS-CoV-2-infected cells, or an animal model with hormonal agents that reduce IRF1 expression, increased insulin / IGF signaling.

“Our findings suggest that SARS-CoV-2 infection disrupts insulin / IGF signaling by increasing IRF1 expression, thereby impairing glycemic metabolism. Decreased IRF1 expression may be reduced by treatment with factors such as dihydrotestosterone and dexamethasone. -19 help. ” Says Shin.

Given the destructive effects that COVID-19 can have on multiple systems, treatment strategies that can reduce the effect of the disease on blood sugar metabolism can be very important. By identifying patients at greater risk of experiencing these effects and intervening to reduce IRF1 activation, some of the severe consequences of COVID-19 in susceptible populations can be prevented.

Decreased blood insulin levels can reduce the risk of COVID-19

more information:
Jihoon Shin et al., SARS-CoV-2 infection disrupts the insulin / IGF signaling pathway in the lung, liver, adipose tissue, and pancreatic cells via IRF1. metabolism (2022). DOI: 10.1016 / j.metabol.2022.155236

Presented by Osaka University

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