HYPERGLYCEMIA AND COVID-19 – TWO SIDES OF ONE COIN

The coronavirus pandemic, which has spread with monstrous rapidity, placed a huge "burden" on humanity. In the attempt to deal with the disease many efforts were directed in the course of unraveling the pathogenetic mechanisms contributing to its adverse complications. The increased frequency of new-onset hyperglycemia during COVID-19 illness gave reason to assume that the SARS-CoV-2 virus could damage the insulin-producing pancreatic beta (β) cells. This fact set a new a focus of research interest related to studying potential mechanisms, leading to hyperglycemia or diabetes mellitus (DM). Literature data indicate that Corona viruses can damage pancreatic β-cells by a direct or indirect mechanism and cause changes in insulin synthesis, secretion and sensitivity. Assessment of the metabolic status of pancreatic β-cells infected with the SARS-CoV-2 virus showed a predominance of the glycolytic metabolic pathway, which further contributed to the worsening of β-cell dysfunction. All these observations give reason to assume that SARS-CoV-2 induces specific morphological and functional changes in pancreatic β-cells, which in long term, would have an impact on the metabolic homeostasis of the individual with a potential risk of future development of DM. In this review, the possible mechanisms of pancreatic β-cell damage are discussed in details, searching the answer to the question of whether SARS-CoV-2 can cause diabetes.