Insulin Resistance
Endocrine Pancreas, Insulin and Glucagon
Insulin Resistance
Insulin resistance is a reduced biological response to insulin in relevant target tissues. Compensatory increases in secretion may initially maintain glucose concentrations despite impaired responsiveness.
Coordinated glucose regulation
Islet output integrates nutrients, autonomic inputs, incretin signals and local cell-to-cell communication. Insulin and glucagon act on different tissues through distinct receptor pathways. Secretion, circulating concentration, insulin sensitivity and glucose disposal are related but separate quantities.
Interpreting the mechanism
Resistance varies across metabolic pathways and organs. Type 2 diabetes develops when insulin secretion becomes insufficient relative to demand, so resistance and diabetes are related but not identical diagnoses.
During movement and recovery
Contracting muscle can increase glucose uptake while circulating insulin declines. Hepatic glucose output and carbohydrate availability help match demand. People using glucose-lowering medicines may have different exercise responses, so general physiology does not replace individualized clinical planning.
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