COVID-19 and diabetes-Two giants colliding: From pathophysiology to management

Abstract

Since December 2019, a new coronavirus, called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread around the world, causing the coronavirus 2019 (COVID-19) pandemic. From the beginning, SARS-CoV-2 has put a strain on the health system. In fact, many patients have had severe forms of the disease with the need for hospitalization due to respiratory failure. To contain the pandemic, the most widely used approach has been lockdowns. Social restrictions have been reduced thanks to the development of vaccines and targeted therapies. However, fatal events still occur among people at high risk of serious infection, such as patients with concomitant diabetes. Different mechanisms have been proposed to explain the poor prognosis of patients with diabetes and COVID-19, but the specific cause is unclear. It is now known that insulin resistance, inflammation, and cytokine storm are involved. Moreover, SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptors to enter cells. This receptor is expressed on pancreatic beta cells and, during infection, it appears that receptor involvement may induce hyperglycemia in patients with or without diabetes. In this study, we discuss the mechanisms underlying the poor prognosis in people with COVID-19 and diabetes and what may improve the outcome in these patients.

Keywords: COVID-19; SARS; blood glucose; diabetes mellitus; lifestyle.

Figure 1

Pathophysiology of diabetes mellitus in patients with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2), which is expressed in several organs, including the lungs, heart, kidneys, liver, and stomach, to enter cells. After endocytosis, SARS-CoV-2 could directly damage pancreatic beta cells as well as induce ACE2 downregulation, which leads to overexpression of angiotensin II with its harmful AT1-mediated effects and increases the levels of proinflammatory cytokines. These virus-induced alterations reduce insulin and augment oxidative stress and insulin resistance.