Type 1 diabetes onset triggered by COVID-19

Expression of SARS-CoV-2 Entry Factors in the Pancreas of Normal Organ Donors and Individuals with COVID-19

“…Autopsy studies of individuals infected with SARS-CoV-2 demonstrate systemic viral dissemination with persistence in multiple organs, including the lungs and kidneys ( Hanley et al., 2020 ; Liu et al., 2020 ; Menter et al., 2020 ; Wichmann et al., 2020 ), but there was an apparent limitation of pronounced inflammatory alterations to the lung and reticulo-endothelial system ( Dorward et al., 2020 ). Recent studies ( Barron et al., 2020 ; Fignani et al, 2020 ; Goldman et al., 2020 ; Holman et al., 2020 ; Li et al., 2020 ; Marchand et al., 2020 ; Unsworth et al., 2020 ; Wang et al., 2020 ) spurred interest in ACE2 expression in the pancreas, particularly the endocrine compartment, to address a potential relationship between diabetes and COVID-19, including the potential for either direct β cell infection or β cell damage via indirect mechanisms. To date, studies of ACE2 expression in the pancreas have been limited and contradictory, and analysis of autopsy specimens from COVID-19 cases have not been published, likely due to challenges associated with tissue procurement and post-mortem autolysis.…”

“…These studies noted elevated serum levels of the exocrine pancreatic enzymes, amylase and lipase, as well as development or worsening of hyperglycemia in SARS-CoV-2-positive individuals ( Wang et al., 2020 ), high prevalence of diabetic ketoacidosis in people hospitalized with COVID-19 ( Goldman et al., 2020 ; Li et al., 2020 ), and increased COVID-19-induced mortality in those with T1D and T2D ( Barron et al., 2020 ; Holman et al., 2020 ). Reports also include increased incidence of new-onset T1D in specific geographic clusters ( Unsworth et al., 2020 ), case reports linking the timing of T1D onset to COVID-19 ( Marchand et al., 2020 ), and pancreatic expression of angiotensin-converting enzyme 2 (ACE2) through which SARS-CoV-2 could gain access to cells ( Chen and Hao, 2020 ), potentially including insulin-producing β cells ( Lee et al., 2020b ; Yang et al., 2020 ). Such reports have collectively led to the hypothesis that SARS-CoV-2 expression in β cells may potentiate or exacerbate T1D or T2D.…”

COVID-19 and diabetes mellitus: from pathophysiology to clinical management

“… 124 ), and patients with newly diagnosed T1DM without ketoacidosis in whom ketoacidosis occurred several weeks after apparent recovery from COVID-19 (ref. 125 ). These findings raise the question as to whether SARS-CoV-2 can trigger this metabolic disease.…”

Diabetes, obesity, metabolism, and SARS-CoV-2 infection: the end of the beginning

“…Severe insulinopenia underlies some of these cases, leading to the suggestion that SARS-CoV-2 infection directly or indirectly compromises β cell function, manifesting in insulin deficiency, hyperglycemia, and ketonemia in susceptible individuals ( Armeni et al., 2020 ). Case reports have described new-onset T1D during the pandemic in some individuals with recent COVID-19 infection, with ( Marchand et al, 2020 ) or without islet antibodies ( Hollstein et al, 2020 ), raising the question of whether SARS-CoV-2 infection may promote insulitis or destruction of islet β cells, possibly via dysregulation of the immune system or direct viral infection of the endocrine pancreas. Indeed, the development of more classical T1D has been temporally associated with exposure to viral infection ( Vehik et al, 2019 ); hence, it seems reasonable to query mechanisms whereby SARS-CoV-2 might trigger insulin deficiency and T1D.…”