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Pharmacological Management of Type 2 Diabetes Mellitus: An APN’s Perspective

Pathophysiology of Type 2 Diabetes Mellitus (T2DM)

Type 2 Diabetes Mellitus is a complex, progressive metabolic disorder characterized by two primary physiological defects: insulin resistance and beta-cell dysfunction.

1. Insulin Resistance: This is often the initial and predominant defect. Insulin is a hormone produced by the beta cells in the pancreas, essential for regulating blood glucose levels. Its main role is to facilitate the uptake of glucose from the bloodstream into cells (muscle, fat, and liver) for energy or storage. In insulin resistance, the body’s cells, particularly in muscle and fat tissue, become less responsive to insulin’s signals. This means that even with normal or even elevated insulin levels, glucose is not effectively cleared from the blood, leading to hyperglycemia (high blood sugar). The pancreas initially tries to compensate by producing more insulin (hyperinsulinemia) to overcome this resistance.

2. Beta-Cell Dysfunction: Over time, the pancreatic beta cells, constantly working overtime to produce excess insulin, become exhausted and eventually lose their ability to produce sufficient insulin. This progressive decline in beta-cell function leads to a relative insulin deficiency. The combination of sustained insulin resistance and impaired insulin secretion results in chronic hyperglycemia.