Diabetes type 2 II: Pathofysiologie

Type 2 diabetes mellitus is a chronic progressive metabolic disorder marked by insulin resistance and progressive pancreatic beta-cell dysfunction, leading to impaired glucose regulation.

Insulin resistance initially develops in the skeletal muscle, liver, and adipose tissue.

Skeletal muscle, the primary site of postprandial glucose uptake, becomes less responsive to insulin, reducing glucose clearance.

Meanwhile, hepatic insulin resistance results in continued glucose production even after meals.

Impaired insulin signaling and dysregulated alpha cells elevate glucagon levels, further increasing hepatic glucose output.

In response, beta cells initially compensate by increasing insulin secretion; however, prolonged exposure to hyperglycemia and metabolic stress progressively impairs beta-cell function.

In adipose tissue, insulin resistance increases lipolysis, elevating circulating free fatty acids, which worsen insulin resistance through lipotoxic effects.

These interconnected metabolic disturbances collectively sustain chronic hyperglycemia.