Diabetes mellitus and COVID-19: Understanding the association in light of current evidence

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections have posed a problematic healthcare situation worldwide since December 2019. Diabetes mellitus is associated with an increased risk and severity of coronavirus disease 2019 (COVID-19). While interacting with various other risk factors, high blood sugar was found to reduce immunity and increase the replication of SARS-CoV-2. Oxidative stress and the release of pro-inflammatory cytokines are greater in diabetic individuals than in healthy people, worsening the outcome of SARS-CoV-2 infection in diabetics. Increased expression of furin and angiotensin converting enzyme 2 (ACE-2) receptor in the hyperglycemic environment may promote the entry of SARS-CoV-2 in the host cell. COVID-19 infection primarily modulates immune and inflammatory responses, and may cause a cytokine storm, resulting in possible lethal outcomes in diabetics. An experimental report suggests that ACE expressed in the pancreas and the SARS-CoV-2 virus invariably destroy β-cells which contain ACE-2 receptors and results in acute diabetes. Moreover, COVID-19 also causes hyperglycemia in an individual with diabetes which may be related to insulin resistance and destruction of β-cells during SARS-CoV-2 infection. Early observations also suggest a correlation between oral hypoglycemic agents and the risk of COVID-19. This review focused on the possible cause and mechanism involved in SARS-CoV-2 infection in diabetics and the role of antidiabetic drugs in COVID-19.

SARS‐CoV‐2 infection and multi-organ system damage: a review

“…High blood glucose has been demonstrated to decrease immunity and increase SARS-CoV-2 replication when combined with other risk factors. In diabetics, oxidative stress and the secretion of pro-inflammatory cytokines are higher than in individuals without DM, exacerbating the result of SARS CoV-2 infection[159].Diabetes, the most frequent endocrine condition, is a face in the "Endocrine phenotype" for COVID-19 since it is one of the most common comorbidities associated with mortality in COVID-19 patients. Most of the available data focused on glucose dysregulation during COVID-19 infection and the development of diabetes[158,159].…”

“…In diabetics, oxidative stress and the secretion of pro-inflammatory cytokines are higher than in individuals without DM, exacerbating the result of SARS CoV-2 infection[159].Diabetes, the most frequent endocrine condition, is a face in the "Endocrine phenotype" for COVID-19 since it is one of the most common comorbidities associated with mortality in COVID-19 patients. Most of the available data focused on glucose dysregulation during COVID-19 infection and the development of diabetes[158,159]. Thus, individuals infected with SARS-CoV-2 should be given extra attention to the emergence of diabetes.Obesity, another metabolic, endocrine condition, increases vulnerability to severe SARS-CoV-2 infection.…”

Levantamento bibliográfico do mecanismo de desenvolvimento de Diabetes Mellitus tipo II após infeção pelo SARS-COV-2

“…Foi observado, também, um perfil hormonal alterado, que demonstra resistência persistente à insulina, onde pacientes que se recuperam de Covid-19 apresentaram perfil hormonal semelhante aos indivíduos com tipo II (Darif, et al, 2021). SARS-COV-2 infecta as células beta-pancreáticas, promovendo hiperestimulação e funcionamento aberrante, fenômenos detectados em pacientes que se recuperam do Covid-19, o que pode, eventualmente, esgotar essas células culminando em morte celular (Sen, et al, 2021).…”

Diabetes Mellitus and COVID-19: Possible Interactions and Mechanisms in Comorbid Patients

“…83 Other studies have reported the expression of high amounts of ACE2 in patients with diabetes, particularly those who were treated with drugs such as angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers. 84,85 The overexpression of ACE2 was suggested to be due to the response from the adaptive immune system to counteract elevated levels of angiotensin-2 and angiotensin-1. By this process, SARS-CoV-2 entrance into cells is facilitated to becomes more severe and fatal in the host cells.…”

“…In another study, SARS-CoV-2 was found to enhance apoptosis of CD4 + T-cells, hence compromising the production of interferon gamma (IFN-γ). 85 Vascular dysfunction and thrombotic complications: Another clinical study found that COVID-19 patients could develop thrombotic diseases like microvascular thrombosis as well as venous or arterial thrombosis. 102 This finding was investigated from a study of necropsy and post-mortem biopsies of persons who died of SARS-CoV-2 infection which found both macro and micro-vascular thrombosis in all the organs analysed.…”