Glycemic control of type 2 diabetic patients with coronavirus disease during hospitalization: a proposal for early insulin therapy

Abstract

TO THE EDITOR: The world is watching the progress of coronavirus disease (COVID᎑19) pandemic. Older age and pre-existing medical conditions, specifically diabetes mellitus, hypertension, ischemic heart disease, and chronic lung disease, are associated with a more severe course of . Diabetes mellitus is one of the most prevalent comorbidities among patients hospitalized due to . Data obtained from 21 hospitals in Wuhan, China, showed that 25% of the reported COVID-19 fatalities had a history of diabetes mellitus (33). Diabetes and ambient hyperglycemia were independent predictors for death and morbidity in patients with severe acute respiratory syndrome (14,34). In this letter, we discuss the putative roles of angiotensin-converting enzyme II (ACE2) in glucose homeostasis in patients with type 2 diabetes and COVID-19 and introduce the proposed benefit of early insulin therapy in patients that warrant hospital care.The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme II (ACE2) receptor for host cell entry and the serine protease TMPRSS2 for virus spike protein priming (16). The binding of SARS-CoV-1 Spike protein to ACE2 activates disintegrin and metalloprotease-17 (ADAM17) and induces ACE2 shedding via a process tightly coupled with TNF-␣ production (15). AD-AM17-mediated ACE2 shedding facilitates SARS-CoV-1 entry and induces tissue damage by TNF-␣ production (15). Interestingly, Kuba et al. (22) found that SARS-CoV-1 infection downregulates ACE2 expression in the mice lungs, and this downregulation was associated with the severity of lung injury. Considering that SARS-CoV-1 and SARS-CoV-2 share Ͼ70% sequence in the Spike protein (31), SARS᎑CoV᎑2 infection might also downregulate the ACE2 expression in the same manner and play a role in the pathological process of the lung injury. ADAM17-mediated ACE2 ectodomain shedding might compromise the renin-angiotensin system (RAS) compensatory axis by impairing ACE2 enzymatic activity or its ability to process angiotensin II on the cell surface. Recently, Monteil et al. (23) showed that human recombinant soluble ACE2 significantly blocks SARS-CoV-2 infections, providing a rationale that soluble ACE2 might not only protect from lung injury but also block the SARS-CoV-2 from entering target cells.ACE2 is expressed in several tissues including the kidney and recognized to be renoprotective by degrading angiotensin II to angiotensin(1-7) (9). The ACE2 receptor protects against lung injury by modulating of the RAS and decreasing angio-tensin II levels (19). Accumulating evidence supports the protective roles of ACE2 in diabetes. ACE2 is expressed in the pancreas and several insulin-sensitive tissues and might play important roles in glucose homeostasis. First, ACE2 deficiency leads to altered glucose metabolism; ACE2-knockout mice showed a ␤-cell defect associated with a decrease in insulin secretion in a manner that is not dependent on angiotensin II but may reflect the collectrin-like action of ACE2 (2, 24). In the db/db mouse...

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“…The number of diabetics in India was 31.7 million in the year 2002, and it is estimated that the number of diabetics in 2030 will be 79.4 million in India (Khatib et al, 2008). In hospitalized patients with COVID 19, DM is the most prevalence co-morbidity (Nakhleh and Shehadeh, 2020). In this review, we discuss the conjectural role of angiotensin-converting enzyme II (ACE2) with type 2 DM and COVID 19.…”

Diabetic Ketoacidosis in Patients With COVID-19

“…Nakhleh and Shehadeh have argued that patients with type 2 diabetes and COVID-19 requiring hospitalization should have early insulin therapy. 6 They suggested that this approach could control hyperglycemia and, in turn, have positive immunomodulatory effects. The complex interactions among ACE 2 cellular receptors and their varying levels in different tissues, circulating ACE 2 released from cellular membranes, angiotensin II, angiotensin 1-7, and SARS-CoV-2 potentially contribute to both viral infection and associated tissue injury and to host defenses.…”