What is the link between diabetes and SARS-CoV-2 infection?

In a recent review published in natural metabolismresearchers investigated whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could promote or trigger development of diabetes Diabetes mellitus (DM).

A recent study reported an increased risk of developing DM after the 2019 coronavirus disease (COVID-19). However, the causality and underlying biological mechanisms are not well characterized. Continued elevation of blood glucose levels after COVID-19 has regressed, possibly due to SARS-CoV-2 infection of non-pancreatic tissues, adds new complexity to deciphering the true link between diabetes and his COVID-19. A dimension has been added.

About reviews

In the current review, researchers assessed the association between COVID-19 and diabetes.

Epidemiological and clinical evidence of diabetes and COVID-19

Multiple studies have reported an increased risk of developing type 1 (T1D) and (T2D) DM after SARS-CoV-2 infection. However, for T1D, epidemiological studies have reported controversial results.

On the contrary, studies using electronic health records have demonstrated an increased risk of developing DM within 12 weeks of SARS-CoV-2 infection, and affected individuals were more likely to develop DM after being diagnosed with SARS-CoV. more likely to receive an insulin prescription within 91 days. – Infections with excessive health burden of new-onset DM and hyperglycemia (>77% of patients had T2D) after 1-year follow-up.

Among several cohorts, 63% to 79% of COVID-19 patients reported improved glycemic control 6 months after recovery and 41% to 79% of COVID-19 patients 10.0 months after recovery improved glycemic control it was done. In contrast, ≤56% of patients had persistent hyperglycemia. A hospitalized SARS-CoV-2-positive patient with acute COVID-19 dysregulation of blood glucose levels returns to physiologically acceptable levels of glycemic control after her 7 months of acute COVID-19 duration indicates that

Dysglycemia may therefore represent a likely aspect of PASC (acute sequelae of COVID-19). However, the diabetogenic effects of COVID-19 may not be a direct result. This is because hyperglycemia has been reported after non-COVID ARDS (acute respiratory distress syndrome), possibly due to systemic inflammation. Nevertheless, her development of T2D and insulin resistance at the PASC stage indicates that COVID-19 may enhance β-cell depletion in high-risk individuals.

Of note, breakthrough infection after COVID-19 vaccination did not significantly reduce the incidence of DM. However, the lower risk of insulin use indicates an improvement in COVID-19 severity and metabolic dysfunction with pre-existing anti-SARS-CoV-2 immunity.

SARS-CoV-2 infection of pancreatic beta (β) cells

Multiple studies have shown that the classical viral entry factors ACE2 and TMPRSS2, in pancreatic β-cells. Furthermore, expression of Neurolipin-1 (ACE2-potentiating factor) indicates an additional pathway for viral entry into pancreatic β-cells. The susceptibility of the pancreatic microvasculature and pancreatic exocrine cells to viral infection may aid viral spread to pancreatic endocrine cells. Still, the virus can cause metabolic alterations associated with pancreatic inflammation.

Studies have reported that COVID-19 deceased infected β-cells, resulting in decreased expression of genes associated with insulin production and release. Specifically, COVID-19 is associated with degranulation, impaired glucose-stimulated insulin secretion, trans- or de-differentiation, and cell death. Moreover, results of recent studies have shown that a significant proportion of islet cells transform into exocrine-like cells during the progression of type 2 diabetes, suggesting that pathological islet plasticity may contribute to β-cell impairment in patients with type 2 diabetes. indicates that it may be the underlying reason for the

Mechanisms of non-pancreatic glucose metabolism disorders

Direct infection of pancreatic β-cells may result in reduced insulin granularity, reduced endocrine function, and decreased de- or trans-differentiation. Adipocyte tissue infection with SARS-CoV-2 reduces adiponectin release, thereby reducing insulin sensitivity. Infection of hepatocytes stimulates gluconeogenesis by promoting glucogenic GP73 secretion. β-cell depletion is also caused by insulin desensitization, gluconeogenesis, and direct β-cell damage.

A study reported that mature adipocytes support replication of SARS-CoV-2, identifying viral proteins in adipocytes of 56.0% of men who died of COVID-19. Of note, the SARS-CoV-2 agent has only been identified among obese men. Adiponectin is characteristic of insulin sensitization, and lack of adiponectin increases general resistance to insulin, according to findings in SARS-CoV-2-positive patients with elevated and decreased levels of C-peptide and adiponectin, respectively. There is a possibility.

Hepatocyte infection with SARS-CoV-2 has been reported to increase glucogenic GP73 activity and promote gluconeogenesis. Conversely, SARS-CoV-2-positive patients report elevated serum GP73 levels that correlate with blood glucose levels.

The review’s findings highlighted a bidirectional relationship between COVID-19 and diabetes mellitus. DM is a common complication associated with the severity of COVID-19, but may be a direct result of SARS-CoV-2 infection. To fully understand biological pathways and conduct population-level and longitudinal studies to facilitate the development and use of targeted interventions for COVID-19 and reduce the associated health burden during the pandemic. is essential.