THE ROLE OF INSULIN RESISTANCE IN THE DEVELOPMENT AND PROGRESSION OF TYPE 2 DIABETES MELLITUS

Type 2 diabetes mellitus is one of the most common endocrine and metabolic disorders and is characterized by chronic hyperglycemia resulting from insulin resistance, progressive pancreatic β-cell dysfunction, and disturbances in glucose and lipid metabolism. The aim of this study was to analyze the role of insulin resistance in the development and progression of type 2 diabetes mellitus. A literature-based analytical approach was used to evaluate the molecular mechanisms of insulin signaling, glucose transport, hepatic glucose production, adipose tissue dysfunction, inflammation, mitochondrial abnormalities, and β-cell compensation. The analysis indicates that insulin resistance usually develops in skeletal muscle, liver, and adipose tissue before persistent hyperglycemia becomes clinically apparent. In the early stages, pancreatic β-cells compensate by increasing insulin secretion. With continued metabolic stress, however, β-cell compensation becomes inadequate, resulting in progressive hyperglycemia. Obesity, visceral adiposity, ectopic lipid accumulation, chronic low-grade inflammation, oxidative stress, and genetic susceptibility contribute to impaired insulin signaling. Insulin resistance therefore represents a central pathophysiological mechanism linking metabolic risk factors with the development of type 2 diabetes mellitus.