Many questions on COVID-19 role in new-onset diabetes

Can COVID-19 disease induce diabetes? It’s a complicated and controversial issue beyond the known effects of the SARS-CoV-2 virus on hyperglycaemia, according to experts.

There’s as much evidence for the expression of ACE2 (angiotensin-converting enzyme 2) in human pancreatic β cells, and a potential portal for SARS-CoV-2, as there is against, according to a Comment article in The Lancet Diabetes and Endocrinology..

And even if the evidence was more consistent, that may not be enough to confirm that COVID-19 causes diabetes, say the US authors.

The article, which reports a summary of the published evidence to date, said there is no consensus regarding which cells within the pancreas express ACE2 and the additional factors or cofactors necessary for effective SARS-CoV-2 entry.

“More than 150 human cell types reportedly express ACE2, with expression levels affected by various factors including age, sex, comorbidities, medications, inflammation, and constituents of the renin–angiotensin system,” the authors said.

They added that ACE2 expression in β cells was expected to be a key feature necessary for the virus to promote diabetes directly.

Although diabetes onset with or soon after acute SARS-CoV-2 infection has been noted in case reports, the epidemiological evidence was also conflicting.

For example, a UK study found type 1 diabetes increased during the COVID-19 pandemic yet a larger German study found no increase.

The authors of the Comment article said the global COVIDIAB registry, whose co-principal investigator is Professor Paul Zimmet from Monash University, may provide more compelling evidence.

“The potential role of SARS-CoV-2 in inducing diabetes is likely to be more complex than the mere notion of pancreatic ACE2 expression and β-cell destruction,” they said.

“As with many clinical scenarios, new-onset diabetes can result from several pathogenic processes involving factors that induce autoimmunity, β-cell stress, or insulin resistance in liver, skeletal muscle, and adipose tissues.”

“Furthermore, β cells could be indirectly damaged as a result of local hypoxia and inflammation due to SARS-CoV-2 infection of the islet microvasculature.”

They concluded that proof of direct toxicity to β cells will require histological evidence of β-cell loss and the presence of SARS-CoV-2 within pancreatic islet cells of COVID-19 patients.

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