Diabetes mellitus is a complex, multifactorial metabolic disease in which insulin resistance and functional impairment of β-cells act as interrelated processes in its pathogenesis. Insulin resistance leads to decreased glucose utilization in peripheral tissues, to which β-cells initially respond with compensatory hypersecretion. However, over time, their structural and functional reserves become exhausted. As a result, chronic hyperglycemia, along with pathobiochemical mechanisms such as lipotoxicity and glucotoxicity, further aggravates β-cell dysfunction. An integrative analysis of these two key components is essential for understanding the progression of diabetes and serves as a theoretical basis for developing individualized therapeutic strategies.

insulin resistance, β-cell dysfunction, hyperglycemia, compensatory hypersecretion, glucotoxicity, lipotoxicity, glucose homeostasis, pathogenesis of diabetes.

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