Recent research suggested that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection might cause metabolic distress, resulting in hyperglycemia in coronavirus disease (COVID-19) patients.
In ten individuals who acquired hyperglycemia following COVID-19, researchers determined the potential indirect and direct effects of SARS-CoV-2 on human pancreatic islets. Although there was no evidence of peripheral anti-islet autoimmunity, the serum of these patients exhibited toxicity on human pancreatic islets, which could be avoided by using anti–interleukin-1β (IL-1β), anti–IL-6, and anti-tumor necrosis factor α, all of which were known to be highly upregulated during COVID-19. Surprisingly, the receptors for those cytokines were abundant on human pancreatic islets.
In some COVID-19 patients, there was a rise in peripheral unmethylated INS DNA, a hallmark of cell death. Pathology of the pancreas from deceased COVID-19-treated hyperglycemic individuals demonstrated moderate lymphocytic infiltration of pancreatic islets and lymph nodes. Furthermore, SARS-CoV-2-specific viral RNA was found in postmortem pancreatic tissues, coupled with the presence of numerous immature insulin granules or proinsulin, indicating β-cell-altered proinsulin processing, as well as β-cell degeneration and hyperstimulation.
These findings suggested that SARS-CoV-2 may have a deleterious impact on human pancreatic islet function and survival by inducing inflammatory conditions, presumably through direct tropism, which may contribute to metabolic abnormalities seen in COVID-19 patients.