Parameters of chronic systemic inflammation in patients with different compensation degree of insulin resistance
- Authors: Zhuravleva Y.A.1, Turyanskaya Y.V.2, Sokolova L.A.2, Gusev E.Y.1
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Affiliations:
- Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences
- Ural State Medical University
- Issue: Vol 28, No 3 (2025)
- Pages: 751-756
- Section: SHORT COMMUNICATIONS
- URL: https://journal-vniispk.ru/1028-7221/article/view/319929
- DOI: https://doi.org/10.46235/1028-7221-17108-POC
- ID: 319929
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Abstract
The paper presents an analysis of systemic inflammatory markers (SIM) in patients with insulin resistance classified into various compensation degrees of chronic metabolic disorders (decompensated and compensated type 2 diabetes mellitus – DM2, prediabetes). Our aim was to analyse the features of chronic SIM marker production in patients with different stages of insulin resistance, i.e., 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 cases with compensated DM2 and 29 persons with decompensated DM2). The control group included healthy blood donors (n = 89). Serum concentrations of C-reactive protein (CRP), interleukins IL- 6, IL- 8, IL- 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 markers of systemic inflammatory response (CRP, IL- 6, IL-8 and TNFα) and microthrombosis (D-dimer). Their production elevated as soon as at the pre-diabetes stage and increased as glycemic disturbances progressed. The increased serum procalcitonin concentration in DM2 is presumably may be caused by translocation of bacterial antigens from the intestine as a result of enterocyte damage. Cortisol levels in most 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 may be considered as a good prognostic sign. In response to metabolic changes, there is a systemic activation of proinflammatory mechanisms since early stages of hyperglycemia, This disorder proceeds with increasing signs of insulin resistance. Indices of systemic inflammatory response and microthrombosis showed the most significant changes.
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##article.viewOnOriginalSite##About the authors
Yulia A. Zhuravleva
Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences
Author for correspondence.
Email: jazhur@mail.ru
ORCID iD: 0000-0003-3266-0954
PhD (Biology), senior research associate, Laboratory of Inflammation Immunology
Russian Federation, EkaterinburgYulia V. Turyanskaya
Ural State Medical University
Email: tiger2003r@mail.ru
PhD (Medicine), Assistant Professor, Department of Hospital Therapy
Russian Federation, EkaterinburgLyudmila A. Sokolova
Ural State Medical University
Email: lasokolova48@mail.ru
ORCID iD: 0000-0002-5931-9417
PhD, MD (Medicine), Professor, Department of Hospital Therapy
Russian Federation, EkaterinburgEugeny Yu. Gusev
Institute of Immunology and Physiology, Ural Branch, Russian Academy of Sciences
Email: gusev36@mail.ru
ORCID iD: 0000-0002-7145-2376
PhD, MD (Medicine), Professor, Chief, Laboratory of Inflammation Immunology
Russian Federation, EkaterinburgReferences
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