Corona infection can trigger diabetes – healing practice

Coronavirus: COVID-19 trigger for diabetes

In the course of the corona pandemic, it has been shown that people with diabetes have an increased risk of severe COVID-19 disease. But vice versa, a severe corona disease can also trigger diabetes. This is shown by scientific studies.

As the University of Basel reports in a recent press release, some COVID-19 patients develop diabetes as a result of the corona infection. An international study with the participation of the University of Basel has now deciphered how the coronavirus SARS-CoV-2 attacks and destroys the insulin-producing cells of the pancreas. The researchers also identified a way to protect these cells.

SARS-CoV-2 can infect the pancreas

Diabetes is considered to be a risk factor for a severe course of illness of an infection with the coronavirus SARS-CoV-2. It is less well known that, conversely, a severe COVID-19 illness can lead to diabetes.

Various studies have shown, however, that an average of around 15 percent of hospitalized COVID-19 patients suffer from newly diagnosed diabetes.

An international research team led by the Stanford University School of Medicine (USA), in which researchers from the University of Basel and the University Hospital Basel were also involved, has now been able to show that the coronavirus can actually infect the beta cells of the pancreas.

The scientists report on this in the journal “Cell Metabolism”. As the communication explains, beta cells produce the hormone insulin, which stimulates tissue cells to take up sugar from the blood – and thereby lower blood sugar.

Tissue samples from the deceased analyzed

Unlike in lung tissue, where SARS-CoV-2 mainly uses a protein called ACE2 as the entry point into the cells, the beta cells of the pancreas have only small amounts of ACE2.

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Therefore, it was previously unclear whether and how the coronavirus penetrates these cells. To answer this question, the researchers analyzed tissue samples from seven deceased COVID-19 patients from Basel.

The analysis showed that SARS-CoV-2 could be detected in the beta cells of the pancreas of the deceased. In addition, these cells contained large amounts of a protein that the virus can use as an entry point as an alternative to ACE2: Neuropilin 1 (NRP1).

Furthermore, laboratory tests with cultured beta cells showed that infected cells produced less insulin and showed signs of death. If the scientists also blocked Neuropilin 1 with an inhibitor, the virus was much less able to penetrate the cells.

Possible protection even in the event of a difficult course

The fact that the infection of the beta cells could be reduced in this way, at least in laboratory tests, shows that these cells could possibly also be protected in patients with a severe course of COVID-19.

“Whether the sugar metabolism will return to normal in all Covid-19 patients after an infection has been overcome and whether and how often persistent diabetes can develop cannot be said with certainty based on the current study situation,” explains pathologist PD Dr. Matthias Matter from the University of Basel and the University Hospital Basel, head of the parts of the study that were carried out in Basel.

According to the information, there are indications that those affected with long COVID, i.e. persistent complaints after the infection, still have diabetes several weeks to months afterwards.

It would therefore make sense to develop a way of preventing permanent damage to the pancreas. (ad)

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Author and source information

This text complies with the requirements of specialist medical literature, medical guidelines and current studies and has been checked by medical professionals.

Swell:

  • University of Basel: Covid-19 can trigger diabetes, (accessed: June 1, 2021), University of Basel
  • Chien Ting-Wu et al.: SARS-CoV-2 infects human pancreatic β-cells and elicits β-cell impairment; in: Cell Metabolism, (veröffentlicht: 18.05.2021), Cell Metabolism

Important NOTE:
This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.

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