Diabetes has become only worse and is the reason behind most of the health conditions in an individual. A diabetic patient’s body cannot convert the blood sugar into the flow of energy in the body due to insufficient insulin (type 1 diabetes) or not good enough use of the insulin released by the pancreas (type 2 diabetes).
Diabetes makes it difficult for the body to transform the consumed food and drink into energy. Thus, the insulin cannot check the blood sugar level increased by consuming food and beverages and becomes an active agent in causing an increase in the body’s blood sugar.
Experts believe that type 2 diabetes is found in 90 percent of the adults in today’s time. Moreover, type 1 & 2 diabetes is thought to be genetic factors or environmental factors by the American Diabetes Association. But a specific form of the virus is considered one of the potential reasons inclusive in the ecological factors causing type 1 diabetes.
Experts circled out this particular virus as one of the reasons triggering diabetes in an individual. The virus, coxsackievirus B type 4 (CVB4), is an enterovirus responsible for causing disease symptoms such as neurologic, respiratory, skin, gastrointestinal, etc. This virus most likely has become the reason to trigger type 1 diabetes in a person.
A group of researchers studied the effects of this virus on a mouse model to understand how viruses like SARS-CoV-2, which is why the current pandemic and downfall of various countries worldwide could lead to the triggering of Diabetes.
The Study on Mouse Model and the Conclusive Events
To understand how enterovirus causes this triggering of Diabetes in an individual, researchers worked and observed a mouse model by planting human pancreatic cells with CVB4 in them, along with human & mouse insulin-producing cells that contained the virus.
After conducting a study on these mice and analyzing a complex reaction inside them, the researchers observed how this virus triggered type 1 diabetes in the mouse. The CVB4 infection downregulates a URI protein responsible for controlling the body’s cellular functions, and then there were several molecular reacting events in the body.
A beta cell in the pancreas is responsible for producing insulin, and the Pdx1 gene regulates this functioning of beta cells. But due to this chain of reacting molecular events, this gene is silenced in the body. The lead author of this research, Dr. Nabil Djouder, who is also a researcher at the Spanish National Cancer Research Center, states about the precise mechanism of this whole experiment in the mouse models and says,
Pdx1 silencing causes the loss of the identity and function of the beta cells, which become more like alpha cells, in charge of increasing blood glucose levels, and hence leading to hyperglycemia and subsequent diabetes, independently of any immune reactions.
The experts also noticed that mice with diabetes showing signs of overexpressing URI protein were more tolerant of blood sugar than other mice groups. There was a correlation between viral particles, URI, and Pdx1 in pancreata from people with diabetes. Hence, it was concluded that there is a common relation between human diabetes and enteroviruses.
Conclusion
Medical professionals use antiviral therapies and drugs to inhibit this silencing of Pdx1 so that diabetes could be treated. The doctors use DNA methyltransferase inhibitors, according to researchers, that helps in inhibiting a protein involved in silencing the Pdx1, ‘ reinstated Pdx1 expression and glucose tolerance in diabetic mice’.
The experts believe that this theory could be validated on the COVID virus, too, as it has been affecting patients with diabetes. The lead author of the study says,
Similarly to our investigations on enteroviruses, some recent clinical observations have associated SARS-CoV-2, the virus responsible for COVID-19, to diabetes in infected patients.
Since the receptor of SARS-CoV-2 is present in beta cells, it would be interesting to study if this virus also alters URI function and silences the expression of Pdx1 to affect beta cell function, promoting diabetes.
Hence, this study could become a potential theory for understanding the COVID virus and how it triggers diabetes in a patient during the pandemic.
