GLOSSARY

Insulin-Mediated Glucose Uptake is increased glucose entry into responding tissue through insulin signaling.

Insulin is secreted by pancreatic beta cells and coordinates nutrient use and storage rather than simply being a fat-making hormone. Important effects include muscle and adipose glucose uptake, suppression of hepatic glucose production and regulation of lipolysis. Not every cell needs insulin for glucose entry. Postmeal concentrations vary with meal composition, tissue sensitivity and clearance, so one insulin excursion cannot determine overall dietary quality or an athlete's nutritional needs.

Muscle contraction can increase GLUT4 trafficking and glucose uptake through partly insulin-independent routes. Circulating insulin may decline during activity while muscle glucose use rises, so lower insulin does not universally imply lower glucose use. Recovery can also change sensitivity. Exercise type, surrounding meals and glucose-lowering medication alter interpretation; physiological changes in healthy exercise should not be transferred directly to medication management or disease without individualized clinical context.

Whole-body, liver, muscle and adipose insulin sensitivity are not one interchangeable measurement. Suppression of glucose production matters in liver, stimulation of uptake in muscle and suppression of lipolysis in adipose tissue. Resistance can differ between tissues and coexist with compensatory secretion. One fasting test without method and context cannot map the entire condition, and a postexercise change is not automatically evidence of disease or a need to eliminate carbohydrate.