Insulinsvaret

Insulinsvaret refers to the body’s physiological response to insulin, encompassing the cellular signaling triggered by insulin binding to its receptor and the downstream metabolic effects that follow. The term is commonly used in Swedish-language literature to describe both the signaling cascade and the systemic outcomes of insulin action.

Mechanistically, insulin binds to the insulin receptor on target cells, activating its tyrosine kinase activity and leading to phosphorylation of insulin receptor substrates. This initiates the PI3K–AKT signaling pathway, which promotes the translocation of GLUT4 transporters to the cell surface in muscle and adipose tissue, increasing glucose uptake. Insulin also suppresses hepatic glucose production and promotes glycogen synthesis in liver and muscle, as well as lipogenesis and, to a degree, protein synthesis. Collectively, these effects constitute the insulinsvaret.

The magnitude and efficiency of insulinsvaret vary between individuals and over time. Factors affecting it include insulin sensitivity, receptor density and signaling efficiency, adiposity, physical activity, age, and genetic background. Counterregulatory hormones such as glucagon, epinephrine, and cortisol can oppose insulin signaling, influencing the overall response.

Clinical relevance lies in conditions where insulinsvaret is altered. Insulin resistance and type 2 diabetes are characterized by impaired signaling and a compensatory rise in insulin levels, while type 1 diabetes involves insufficient endogenous insulin, reducing the insulinsvaret. Assessment methods range from research-based techniques like the hyperinsulinemic-euglycemic clamp to surrogate measures such as HOMA-IR and QUICKI.