PARAMETERS OF CHRONIC SYSTEMIC INFLAMMATION IN PATIENTS WITH DIFFERENT DEGREES OF COMPENSATION OF INSULIN RESISTANCE



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Abstract

Abstract

The paper presents an analysis of systemic inflammatory markers in patients with insulin resistance leading to chronic metabolic disorders of various compensation degrees (decompensated and compensated type 2 diabetes mellitus - DM2, prediabetes). The aim: to analyse the features of chronic systemic inflammation marker production in patients with different stages of insulin resistance: prediabetes, compensated DM2 and decompensated DM2. Materials and Methods. The study included patients with hyperglycemia, who were divided into 3 groups according to blood glucose and glycated hemoglobin levels: 26 patients with prediabetes, 34 patients with compensated DM2 and 29 patients with decompensated DM2. The control group included healthy blood donors (n=89). Serum concentrations of C-reactive protein (CRP), interleukins (IL)-6, -8, -10, tumor necrosis factor alpha (TNFα), D-dimer, troponin I, myoglobin, cortisol, and procalcitonin were determined by enzyme immunoassay. The results of the study showed that most markers of systemic inflammation in all three groups of patients with pathological insulin resistance exceeded those in the control group. The most intense variations were observed with the indices of systemic inflammatory response (CRP, IL-6, IL-8 and TNFα) and microthrombosis (D-dimer). Their production elevated already at the pre-diabetes stage and increased as glycemic disturbances progressed. The increased PCT serum concentration in DM2 is presumably due to translocation of bacterial antigens from the intestine as a result of enterocyte damage. Cortisol levels in the majority of patients remained within reference values and did not differ significantly depending on the stage of insulin resistance. The same trend was observed for systemic alteration markers - myoglobin and troponin I, which can be considered as a good prognostic sign.  Conclusion. In response to metabolic changes already at the early stages of hyperglycemia there is a systemic activation of proinflammatory mechanisms, which progresses with increasing signs of insulin resistance.

About the authors

Yulia Zhuravleva

Institute of Immunology and Physiology of UB RAS, Yekaterinburg, Russian Federation

Email: jazhur@mail.ru
ORCID iD: 0000-0003-3266-0954
SPIN-code: 1408-5218
Scopus Author ID: 57216158631
ResearcherId: AAK-5463-2021

PhD, senior research associate, laboratory of inflammation immunology

Russian Federation, 620078,Russia, Ekaterinburg, Pervomayskaya str., 106

Yulia Turyanskaya

Ural State Medical University Yekaterinburg, Russian Federation

Email: tiger2003r@mail.ru
SPIN-code: 2745-8710

PhD, department assistant of the Hospital therapy department

Russian Federation, 620028, Russia, Ekaterinburg, Repina str., 3

Lyudmila Sokolova

Ural State Medical University Yekaterinburg, Russian Federation

Email: lasokolova48@mail.ru
ORCID iD: 0000-0002-5931-9417
SPIN-code: 6461-3694
Scopus Author ID: 57196403406
ResearcherId: E-2555-2018

MD, professor, professor of the Hospital therapy department

Russian Federation, 620028, Russia, Ekaterinburg, Repina str., 3

Eugeny Gusev

Institute of Immunology and Physiology of UB RAS, Yekaterinburg, Russian Federation

Author for correspondence.
Email: gusev36@mail.ru
ORCID iD: 0000-0002-7145-2376
SPIN-code: 3296-6597
Scopus Author ID: 7102224286
ResearcherId: AAE-1536-2021

MD, professor, Chief of the laboratory of inflammation immunology

Russian Federation, 620078,Russia, Ekaterinburg, Pervomayskaya str., 106

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Copyright (c) Zhuravleva Y., Turyanskaya Y., Sokolova L., Gusev E.

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