ABSTRACT
Introduction
The COVID-19 pandemic has changed the landscape of modern medicine on a global scale. An emerging concern is the recognition of a bidirectional relationship between COVID-19 and diabetes. Diabetes is a risk factor for severe COVID-19 illness. Intriguingly, recent epidemiological and in vitro studies suggest that infection with SARS-CoV-2, the causative viral agent of COVID-19, is associated with new-onset diabetes and worsening diabetes control. These factors have affected the management of diabetes.
Areas covered
This review provides an overview of our current understanding of the incidence and prevalence of diabetes in relation to the COVID-19 pandemic, highlights studies evaluating SARS-CoV-2’s beta cell tropism and its effects on insulin secretion and sensitivity and evaluates the impact of the pandemic on diabetes management and metabolic control.
Expert opinion
Epidemiological studies have noted an increase in the incidence of new-onset diabetes associated with COVID-19 in patients with phenotypes of type 1 diabetes, type 2 diabetes and Ketosis-Prone Diabetes. Prospective studies are needed to fully elucidate the association between COVID-19 and diabetes and to characterize persons at risk of developing diabetes after SARS-CoV-2 infection, identify those who should be screened for diabetes, and determine the natural histories of different forms of diabetes associated with COVID-19.
Plain Language Summary
The COVID-19 pandemic has affected medical care worldwide. Healthcare systems have been overwhelmed during ‘surges’ of COVID-19 illness, and access to care has been affected during prolonged lockdowns. COVID-19 is caused by the SARS-CoV-2 virus, which is highly contagious. Infection with SARS-CoV-2 can lead to serious illness, primarily in the lungs, but it often affects many other organ systems, leading to disability and death. Recent studies show that persons with diabetes can have a more severe course of illness if infected with SARS-CoV-2. There is also growing evidence that COVID-19 may cause diabetes or worsen preexisting diabetes. In this review, we discuss the findings of studies that show an increase in the frequency of diabetes diagnosed worldwide during the COVID-19 pandemic. We also examine recent data that suggest SARS-CoV-2 can infect and damage the insulin-producing cells in the pancreas. Finally, we provide an overview of the impact of COVID-19 on the management of patients with diabetes, and the emerging use of telemedicine in diabetes care.
Article highlights
The incidence of type 1 diabetes (T1D), type 2 diabetes (T2D) and atypical forms of diabetes presenting with DKA has increased during the pandemic as compared to pre-pandemic levels in both pediatric and adult patients.
Diabetes is a major risk factor for hospitalization due to COVID-19; new-onset hyperglycemia in patients without diabetes increases the severity of COVID-19 illness.
Retrospective studies comparing patients with and without COVID-19 demonstrate an increase in new-onset diabetes.
SARS-CoV-2 infects host cells via ACE2; SARS-CoV-2 has been shown to infect pancreatic beta cells resulting in impaired insulin secretion, apoptosis, and beta cell injury.
SARS-CoV-2 infection promotes insulin resistance by activating the integrated stress response and downregulating insulin signaling pathways. SARS-CoV-2 also has been shown to infect adipocytes and lead to adipose dysfunction and decreased adiponectin secretion.
Glycemic control and parameters affecting glycemic control (such as weight management, management of complications and physical activity) have been variably affected in different parts of the world and within populations.
Health care providers have had to adapt to periods of overwhelming demand, limited healthcare resources, personnel and quarantine restrictions; telemedicine has facilitated positive diabetes management.
Further studies are required to understand ‘Long COVID’ and the pathophysiology and natural history of new-onset diabetes caused by COVID-19 illness.
Declaration of interest
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.