Аңдатпа
Type 2 diabetes mellitus is a multifactorial metabolic disorder characterized by insulin-independent hyperglycemia, impaired carbohydrate and lipid metabolism, and systemic complications. This study aimed to investigate metabolic and immune alterations in male laboratory rats with experimentally induced T2DM. Forty rats weighing 200 ± 20 g were divided into two groups: control and T2DM. Diabetes was induced via a single intraperitoneal injection of streptozotocin (30 mg/kg), and hyperglycemia was confirmed by fasting blood glucose levels exceeding 7.0 mmol/L. Metabolic analysis revealed significant hyperglycemia (20% increase, p<0.05), elevated immunoreactive insulin and C-peptide concentrations (p<0.05), and a trend toward increased glycated hemoglobin (HbA1c), indicating compensatory β-cell hyperactivity and early-stage metabolic dysregulation. Immunological assessment showed decreased total leukocyte and lymphocyte counts, with pronounced reductions in T-lymphocytes (CD3+) and T-helper cells (CD4+) (p<0.05), while T-suppressor cells (CD8+) remained unchanged, resulting in a reduced CD4/CD8 ratio. Functional tests demonstrated impaired lymphocyte mitogenic response, reduced antibody-forming cell activity, and suppressed natural killer cell activity (p<0.01), suggesting compromised innate and adaptive immunity. These findings indicate that experimental T2DM induces a combination of metabolic disturbances and systemic immune dysfunction. The observed interplay between hyperglycemia, β-cell stress, and immune suppression may contribute to increased susceptibility to infections and chronic inflammatory processes. Understanding these early alterations provides insight into the pathogenesis of T2DM and may inform the development of therapeutic strategies targeting both metabolic and immune pathways.