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Covid can infect insulin-producing cells in pancreas, research shows

Covid can infect insulin-producing cells in pancreas, research shows

STUDIES have revealed that Covid-19 can infect insulin-producing cells in the pancreas and alter their function, possibly explaining why some people develop diabetes due to the virus, according to a report in The Guardian.

Amid the pandemic, there has been a rise in the number of patients who have developed diabetes due to Covid.


In order to identify which organs could be infected by Covid, Prof Shuibing Chen at Weill Cornell Medicine in New York screened various cells and organoids – lab-grown clusters of cells that mimic the function of organs, The Guardian report added.

The results showed that lung, colon, heart, liver, and pancreatic organoids could all be infected, as well as dopamine-producing brain cells.

Further experiments showed that insulin-producing beta cells within the pancreas were also susceptible, and that once infected, these cells produced less insulin.

According to the newspaper report, these cells also produce less hormones usually manufactured by different pancreatic cells.

The results were presented at the annual meeting of the European Association for the Study of Diabetes.

“They are basically changing their cellular fate, so instead of being hardcore beta cells which secrete a lot of insulin, they start to mix different hormones. It could provide further insight into the pathological mechanisms of Covid-19," Prof Chen was quoted as saying by The Guardian.

However, it's not clear whether the changes due to Covid infection are long-lasting, Prof Chen said.

Another research by Prof Francesco Dotta at the University of Siena in Italy and colleagues showed that people with existing diabetes or prediabetes are at greater risk of pancreatic dysfunction if they catch Covid.

These studies support the rationale that Covid could increase the risk of developing diabetes in people who are either predisposed to it, or even get it from scratch, the report added.

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