Diabetes

Can COVID-19 cause diabetes? | Nature Metabolism

Is COVID-19 capable of inflicting damage on β-cells? We don’t know. Evidence from single-cell RNA surveys available at the outset of the pandemic indicated that the SARS-CoV-2 co-receptor ACE2 is not present in β-cells, whereas the receptor TMPRSS and the newly discovered NRP1 co-receptor are expressed at low levels13. Some surveys of pancreatic islets by immunohistochemistry have yielded results consistent with these findings14,15, whereas others have found SARS-CoV-2 receptors in β-cells16. Could the receptors be induced in β-cells as part of the syndrome? This induction is possible but difficult to demonstrate. In our experience, there is no clear association between diabetic ketoacidosis and readouts of inflammation, such as leukocyte and platelet counts, C-reactive protein, D-dimer and ferritin. However, for the virus alone to cause sufficient loss of β-cell function and impair insulin secretion, the extent of viral entry should be extensive. In addition, if the virus were to cause permanent loss of β-cell function, post-COVID diabetic ketoacidosis should routinely require insulin treatment, which is not the case. Indeed, most instances of ketoacidosis during the acute phase of the illness are mild to moderate. The challenges of treating ketoacidosis in COVID-19 are mostly extrinsic to β-cells: in fluid management, we often must take a narrow path between maintaining organ perfusion and preventing fluid accumulation in the lungs, owing to respiratory distress, stunned heart or outright cardiac injury, and prothrombotic state. Renal tubular damage also leads to protracted and unusual electrolyte abnormalities that can be difficult to manage. In addition, as steroid use to treat COVID-19 has gone mainstream, the recovery of β-cell function is delayed or blunted.In my view, the focus on whether the virus infects β-cells is too narrow. Regardless of the expression levels of SARS-CoV-2 co-receptors, evidence of viral infections causing permanent β-cell damage is scant17. Stress-induced hyperglycaemia associated with infection is generally transient. Only in patients predisposed to developing type 1 diabetes has an intercurrent viral illness been suspected to deliver the final blow to faltering β-cell function. In this regard, if COVID-19 were in fact to cause permanent insulin-dependent diabetes, SARS-CoV-2 would be unique. Data on SARS1 are inconclusive in this regard18. However, if COVID-19 were to cause β-cell loss in patients with a predisposed autoimmune milieu, we would have seen an excess incidence of type 1 diabetes in association with the pandemic. The limited data in this regard do not bear out this interpretation19. However, we might possibly be undercounting the incidence of type 1 diabetes, because patients tend to avoid treatment at large academic medical centres and are more likely to seek care from primary providers. Recent evidence indicating genetic autoimmune susceptibility to respiratory failure in patients with COVID-19 (ref. 20) provides a blueprint for studies addressing the role of type 1 diabetes autoimmunity in COVID-19-associated ketoacidosis. However, whether there are enough patients to conduct such a study is unclear.

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