We have detected that you are using an Ad Blocker. PracticeUpdate is free to end users but we rely on advertising to fund our site. Please consider supporting PracticeUpdate by whitelisting us in your ad blocker.
We have sent a message to the email address you have provided, . If this email is not correct, please update your settings with your correct address.
The email address you provided during registration, , does not appear to be valid. Please update your settings with a valid address before to continue using PracticeUpdate.
Welcome to PracticeUpdate! We hope you are enjoying access to a selection of our top-read and most recent articles. Please register today for a free account and gain full access to all of our expert-selected content.
You can find your saved items on your dashboard, in the "saved" tab.
You've recommended your first item
Your recommendations help us improve our content suggestions for you and other PracticeUpdate members.
You've subscribed to your first topic alert
What does that mean?
Each day, we'll check to see if new items have been published to the topics you're subscribed to, and we'll send you one email with all of the new items from that day.
We'll keep all topic alert notifications available on your dashboard for 30 days, to make sure you don't miss anything.
Lastly, whenever you have unread items in the topics you've subscribed to, the "Alerts" icon will light up in the main menu. Just click on the bell to see your five most-recent, unread notifications.
In this commentary, the authors discuss whether COVID-19 can lead to new-onset diabetes. They note that COVID-19 infection, like other infections, can cause hyperglycaemia in individuals without known diabetes, and they highlight potential mechanisms through which this could occur. Reports on the onset of type 1 diabetes due to COVID-19 have been conflicting, and the authors conclude that a causal association is unlikely. Data regarding angiotensin-converting enzyme 2 (ACE2) expression on pancreatic cells have also been conflicting. Further, it remains unclear if beta cells express or can be induced to express the necessary receptor for direct viral injury and beta-cell destruction. Beyond ACE2 expression and direct beta-cell effects, the authors discuss other mechanisms that could result in new-onset diabetes in the setting of COVID-19.
Available data regarding the effects of COVID-19 on the development of new-onset diabetes are conflicting, and further studies are needed.
Reports noting the deleterious impact of diabetes on people infected with SARS-CoV-2 arose in the earliest weeks of the COVID-19 pandemic.1 Over time, obesity, hyperglycaemia, type 2 diabetes, and type 1 diabetes have each been reported to be associated with increased COVID-19 morbidity and mortality, as well as expanded therapeutic needs during hospital admission.2 More controversial, however, has been the question of whether SARS-CoV-2 specifically is, in and of itself, capable of inducing diabetes; and, if so, in which of its forms.3 Beyond this question, hypotheses abound as to whether such a disease-provoking activity (if it exists) is due to acceleration of an underlying and potentially pathogenic feature associated with traditional diabetes pathogenesis (ie, type 1 or type 2 diabetes), or incitement of a new variant of diabetes involving either acute β-cell destruction or impairment of insulin secretion.4 What does seem clear is that SARS-CoV-2 infection, like many other infections, has the ability to induce hyperglycaemia in people without a previous diagnosis of diabetes, be it through diminished insulin secretion, enhanced release of counter-regulatory hormones, excessive hepatic glucose production, impaired glucose disposal, or a combination of these factors.3, 4