Atherogenic insulin resistance indices and immune disturbances in COVID–19

Background: It is now proven that insulin resistance occurring during SARS-CoV-2 infection is the major cause for the hyperglycemia observed, and it can even persist long after recovery. The precise mechanisms of insulin resistance, whether new-onset or pre-existing, remain largely a mystery. Chronic immune dysregulation, persistent subclinical inflammation, adipose tissue dysfunction and pro-inflammatory cytokines are thought to be of fundamental importance. The current study aims to investigate the role of SARS-CoV-2 infection and the related inflammation in the pathogenesis of insulin resistance in different types of newly emerging disorders of carbohydrate metabolism following infection. Methods and materials: The current study included 168 patients (59 males and 109 women; mean age 54.04 ± 8.08 years), divided into three groups: group 1 (patients with active COVID-19 infection; n = 100), group 2 (individuals with newly diagnosed carbohydrate disorders after proven COVID-19 or post-COVID group; n = 35) and group 3 (COVID-19 negative subjects with Metabolic Syndrome; n = 33). Standard biochemical and immunological parameters were measured, and atherogenic indices for IR (TyG index and TG/HDL-C ratio) were calculated using the corresponding formula. Results: Patients with active coronavirus infection demonstrated the highest levels of TyG index and TG/HDL-C ratio, which differed significantly from both the reference COVID-negative group and from the Post-COVID group (p < 0.05). Among the individuals in the post-COVID group, we found a positive correlation between TyG index and IL-10 (r = 0.481; p = 0.008), IL-17A (r = 0.384; p = 0.048) and HCF-D (r = 0.387; p = 0.038). In the same group, the TG/HDL-C ratio positively correlated with CD8 (r = 0.648; p < 0.001), TNF-α (r = 0.559; p < 0.001), IL-10 (r = 0.954; p < 0.001), 8-Epi-PGF2α (r = 0.451; p = 0.006) and HIF-1α (r = 0.863; p < 0.001). Conclusion: Immune dysregulation, along with oxidative stress and cellular hypoxia observed during and after infection, seems to be implicated in the genesis, maintenance and progression of the insulin resistance (IR). IR, as measured by widely used atherogenic indices, is present not only during the COVID-19 course but also in cases of newly emerging carbohydrate disorders following infection, including T2DM, prediabetes, and T1DM.