促炎细胞因子
医学
大流行
糖尿病
免疫学
冠状病毒
1型糖尿病
胰岛素抵抗
2型糖尿病
疾病
2019年冠状病毒病(COVID-19)
炎症
内科学
传染病(医学专业)
内分泌学
作者
Jonathan Mannheim,Daniel Y. Johnson
出处
期刊:Pediatric Annals
[SLACK, Inc.]
日期:2024-07-01
卷期号:53 (7)
标识
DOI:10.3928/19382359-20240502-07
摘要
Past literature on the development of type 1 diabetes (T1D) and type 2 diabetes (T2D) has emphasized the influence of exogenous factors, including viral infections, in the development of these conditions. The coronavirus disease 2019 (COVID-19) pandemic again highlighted the complicated connection between viral infection and the development of diabetes. The complex interplay of proinflammatory, genetic, and socioeconomic factors can help explain the increased incidence of T1D and T2D during the pandemic. Proposed pathophysiological mechanisms connecting severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to T1D include the expression of angiotensin enzyme 2 receptors on pancreatic islet cells, resultant proinflammatory states, and potential transient damage caused by viral entry. The intricate web of genetic factors, social determinants of health (including the rise of obesity), and the impact of proinflammatory states during SARS-CoV-2 infection on insulin resistance suggests mechanisms linking SARS-CoV-2 infection to the development of diabetes. [ Pediatr Ann . 2024;53(7):e258–e263.]
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