Comprehensive Analysis Of Biochemical Alterations And Hemostatic Dysfunction In Dexamethasone- And Streptozotocin-Induced Type 2 Diabetes Mellitus Models
Abstract
Diabetes mellitus remains one of the most significant medical and social problems of modern healthcare due to the steadily increasing prevalence, high rate of chronic complications, and its substantial impact on patients’ quality of life and life expectancy. Experimental models of diabetes, particularly dexamethasone- and streptozotocin-induced models, are widely used to investigate the pathogenetic mechanisms of the disease and to evaluate the efficacy of novel therapeutic approaches. The dexamethasone-induced model is characterized by the development of insulin resistance, hyperglycemia, and disturbances in lipid metabolism, resulting from glucocorticoid-induced suppression of peripheral tissue sensitivity to insulin and enhanced hepatic gluconeogenesis. In contrast, streptozotocin exerts a cytotoxic effect on pancreatic β-cells, leading to their destruction and the development of relative or absolute insulin deficiency. The combined use of these models allows a more comprehensive reproduction of the key pathogenetic features of type 2 diabetes mellitus and provides deeper insight into the mechanisms underlying metabolic dysfunction.
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