Type 2 Diabetes Mellitus

Type 2 diabetes mellitus develops when insulin resistance in skeletal muscle, liver, and adipose tissue is followed by progressive pancreatic beta-cell dysfunction. Muscle takes up less glucose, the liver releases more glucose between meals, and adipose tissue contributes to abnormal free-fatty-acid signalling. The result is sustained hyperglycemia rather than a brief post-meal rise. The process usually evolves quietly. A person may have elevated glucose for years before diagnosis, and beta-cell function continues to decline after diagnosis. That progression explains why lifestyle measures and one medication may work initially but later require combination therapy or insulin. It is not a treatment failure; it reflects the biology of the disease. The clinical task is therefore broader than lowering a glucose value. Treatment must reduce microvascular injury, cardiovascular events, kidney failure, hypoglycemia, treatment burden, and symptomatic hyperglycemia while matching the person's function, preferences, comorbidities, and ability to access therapy.