Quantifiable assessments used to determine the responsiveness of peripheral tissues, primarily muscle and adipose cells, to circulating insulin levels. High sensitivity implies efficient glucose uptake with minimal required insulin, whereas low sensitivity, or resistance, necessitates hyperinsulinemia to maintain euglycemia. These metrics are central to diagnosing prediabetes and metabolic syndrome. Understanding this responsiveness is key to optimizing glucose homeostasis.
Origin
The term originates in diabetology and endocrinology, focusing on the post-receptor events following insulin binding. ‘Sensitivity’ refers to the dose-response relationship of insulin action, contrasting with measures of insulin secretion itself. Metrics are derived from controlled infusion studies or surrogate markers like HOMA-IR.
Mechanism
Insulin sensitivity is fundamentally determined by the density and function of the insulin receptor and downstream signaling molecules, particularly IRS proteins and GLUT4 translocation machinery. Reduced sensitivity often involves chronic inflammatory states or lipid overload impairing these intracellular phosphorylation events. Enhancing these metrics requires optimizing cellular lipid handling and reducing systemic inflammatory load to restore signal transduction fidelity.
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