Abstract
The infection with SARS-CoV-2 impairs the glucose–insulin axis and this contributes to oxidative (OS) and nitrosative (NSS) stress. Here, we evaluated changes in glucose metabolism that could promote the loss of redox homeostasis in COVID-19 patients. This was comparative cohort and analytical study that compared COVID-19 patients and healthy subjects. The study population consisted of 61 COVID-19 patients with and without comorbidities and 25 healthy subjects (HS). In all subjects the plasma glucose, insulin, 8-isoprostane, Vitamin D, H2S and 3-nitrotyrosine were determined by ELISA. The nitrites (NO2−), lipid-peroxidation (LPO), total-antioxidant-capacity (TAC), thiols, glutathione (GSH) and selenium (Se) were determined by spectrophotometry. The glucose, insulin and HOMA-IR (p < 0.001), 8-isoprostanes, 3-nitrotyrosine (p < 0.001) and LPO were increased (p = 0.02) while Vitamin D (p = 0.01), H2S, thiols, TAC, GSH and Se (p < 0.001) decreased in COVID-19 patients in comparison to HS. The SARS-CoV-2 infection resulted in alterations in the glucose–insulin axis that led to hyperglycemia, hyperinsulinemia and IR in patients with and without comorbidities. These alterations increase OS and NSS reflected in increases or decreases in some oxidative markers in plasma with major impact or fatal consequences in patients that course with metabolic syndrome. Moreover, subjects without comorbidities could have long-term alterations in the redox homeostasis after infection.
Highlights
The presence of anti-N protein, and anti-S protein antibodies of the SARS-CoV-2 virus was determined at the time of admission of the patients
In most of the patients, antibodies against these proteins were present at the time of admission and in the rest of them, the antibodies appeared a few days later
During the analytical validation of the ELISA to measure anti-N protein antibodies, it was found that up to 11% of subjects may not have measurable amounts of anti-N protein antibodies at the time of the manifestation of clinical symptoms
Summary
COVID-19 impairs glucose homeostasis and metabolism in non- and diabetes mellitus (DM) and metabolic syndrome (MS) patients due to the cytokine storm, inflammation, angiotensin II-converting enzyme (ACE2) down-regulation and the direct injury to the pancreatic β-cells [2]. It deteriorates the already impaired glucose homeostasis in patients with DM and in patients with other comorbidities such as obesity, insulin resistance (IR), hyperinsulinemia and hypertension in whom alterations in insulin secretion are already present and contribute to hyperglycemia [3]. Increased inflammation and massive production of cytokines generate IR which adds to the deterioration of the insulin secretion by β-cells [4]
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