4.6 Article

SARS-CoV-2 Infection and Pancreatic β Cell Failure

Journal

BIOLOGY-BASEL
Volume 11, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/biology11010022

Keywords

virus; diabetes; COVID-19; SARS-CoV-2; pancreas; beta cell

Categories

Funding

  1. Japan IDDM Network Research Grant
  2. Japan Diabetes Foundation

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This article provides a comprehensive review of the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic beta-cell damage leading to the onset of diabetes. It discusses the findings from published studies and highlights the need for further research in understanding the pathogenesis of diabetes mellitus.
Simple Summary: Accumulating evidence suggests that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may have the potential to induce pancreatic beta-cell damage, leading to diabetes onset in patients with coronavirus disease 2019 (COVID-19). However, controversial results have been reported among study groups. Here, we provide a comprehensive review of published findings that describe the potential relationship between SARS-CoV-2 infection (COVID-19) and pancreatic beta-cell failure, and how this may contribute to the development of diabetes. SARS-CoV-2 infection primarily causes pulmonary symptoms; however, accumulating reports indicate that some patients with COVID-19 have multiple organ dysfunction or failure. Although diabetes is considered a risk factor for severe COVID-19, SARS-CoV-2 infection may also be a causal factor for diabetes mellitus in patients with COVID-19. According to the research reviewed in this paper, the pancreas and pancreatic beta cells appear to be targets of SARS-CoV-2 and are damaged by direct or indirect effects of the infection. However, controversial results have been reported between study groups, mainly due to the limited number of cases with diabetes precipitated by COVID-19. In this review, we comprehensively discuss the published findings on the potential association between SARS-CoV-2 infection or COVID-19 and pancreatic beta-cell damage leading to diabetes onset. These findings will further contribute to our understanding of the pathogenesis of diabetes mellitus.

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