Intertwined pathways of SARS-CoV-2 infection and its clinical repercussions on glucose homeostasis: Exploring the rise of new-onset diabetes

Abstract

Coronavirus disease 2019 (COVID-19) and diabetes seem to have a bidirectional relationship. People suffering from diabetes mellitus (DM) are at higher risk than non-diabetics to contract SARS-CoV-2 infections and acquire COVID-19-related health issues. Diabetes is consistently linked to higher disease risk and death among COVID-19 patients. Data also suggest that multiple phenotypic expression alterations caused by SARS-CoV-2 could complicate the pathogenesis of pre-existing diabetes or result in additional pathological conditions. Clinical research data shows that SARS-CoV-2 infection promotes metabolic abnormalities in humans. Furthermore, recent studies concerning new-onset diabetes (NOD) in COVID-19 affected population, who had previously been infected with the virus, reinforce the notion that SARS-CoV-2 has a direct influence on glucose metabolism. Data from various sources indicated that SARS-CoV-2 infected individuals had a greater prevalence of Diabetic Ketoacidosis (DKA), which might be related to a blatant assault on the beta (β)cells of the pancreas. This virus has also been attributed to binding with the ACE 2 receptors found in critical body tissues as well as organs such as β islet cells of the pancreas, small intestine, kidneys and adipose tissues, causing Ketosis-prone diabetes (KPD), which is a very prevalent form of diabetes in Asia, especially India. It has been observed that despite the lack of autoantibodies, the people so affected experience short, transitory insulin deficit that produces DKA at first, but they recover from this β-cell secretory failure over time. This paper highlights the complex interplay between SARS-CoV-2 and its clinical implications on diabetic pathobiology, emphasizing how the cause-effect relationship operates bidirectionally between the two.