The COVID-19 Pandemic during the Time of the Diabetes Pandemic: Likely Fraternal Twins?

Abstract

An altered immune response to pathogens has been suggested to explain increased susceptibility to infectious diseases in patients with diabetes. Recent evidence has documented several immunometabolic pathways in patients with diabetes directly related to the COVID-19 infection. This also seems to be the case for prediabetic subjects with proinflammatory insulin resistance syndrome accompanied with prothrombotic hyperinsulinemic and dysglycemic states. Patients with frank hyperglycemia, dysglycemia and/or hyperinsulinemia develop systemic immunometabolic inflammation with higher levels of circulating cytokines. This deleterious scenario has been proposed as the underlying mechanism enhancing a cytokine storm-like hyperinflammatory state in diabetics infected with severe COVID-19 triggering multi-organ failure. Compared with moderately affected COVID-19 patients, diabetes was found to be highly prevalent among severely affected patients suggesting that this non-communicable disease should be considered as a risk factor for adverse outcomes. The COVID-19 pandemic mirrors with the diabetes pandemic in many pathobiological aspects. Our interest is to emphasize the ties between the immunoinflammatory mechanisms that underlie the morbidity and lethality when COVID-19 meets diabetes. This review brings attention to two pathologies of highly complex, multifactorial, developmental and environmentally dependent manifestations of critical importance to human survival. Extreme caution should be taken with diabetics with suspected symptoms of COVID-19 infection.

Responses to acute infection with SARS-CoV-2 in the lungs of rhesus macaques, baboons and marmosets

“…Baboons developed more-severe inflammatory lesions compared with macaques. Baboons are also a preferred model for cardiovascular and metabolic diseases including diabetes [27][28][29] ; further development of the baboon model may therefore prove especially useful for the study of such comorbidities with COVID-19.…”

Clinical Features of COVID-19 Patients with Diabetes and Secondary Hyperglycemia

“…Hyperglycemia and diabetes are linked with chronic low-grade inflammatory processes and related vulnerability to infection, which can impair antiviral activity and increase the risk for fatality [ 31 ]. Chronic inflammation perhaps acts as the underlying mechanism enhancing a cytokine storm hyperinflammatory state that triggers multiorgan failure in COVID-19-infected individuals [ 32 ]. Therefore, patients with T2DM are characterized by a pervasive status of low-grade inflammation coupled by a progressive decline of immune system function evidenced by abnormal T cell subsets.…”

Pathophysiology of COVID-19: Mechanisms Underlying Disease Severity and Progression

“…Although direct damage of pancreatic β-cells has been proposed as a plausible mechanism behind this phenotype, immune destruction of β-cells has also been suggested in addition to bystander death due to exocrine infection ( 101 ). Importantly, COVID-19 appears to enhance complications in patients with diabetes, likely due to viral-induced pancreatic dysfunction as well as associated immune dysregulation, vasculopathy, and coagulopathy ( 29 , 37 ).…”