GLOSSARY

Glucose-Stimulated Insulin Secretion (GSIS) is beta-cell secretion following glucose sensing.

Proinsulin processing produces insulin and C-peptide. C-peptide helps assess endogenous secretion but has different clearance from insulin, so concentrations and ratios need clinical context. Early and sustained secretion phases depend on stimulus and test method. One value cannot establish total beta-cell reserve, sensitivity across every tissue or medication need. Interpretation must distinguish secretion, precursor processing and removal rather than treating their biomarkers as identical measurements.

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.

Pancreatic islets contain several signaling cell types with important local interactions. Somatostatin can inhibit other secretions, while pancreatic polypeptide and amylin have distinct roles. Amylin is co-secreted with beta-cell insulin and participates in gastric emptying and meal-ending signals. Similar names or simultaneous secretion do not imply identical effects, receptors or drug uses; each signal needs its source and function distinguished within the islet and gut–brain network.

The incretin effect is greater insulin secretion after oral than intravenous glucose when glycemia is matched. GLP-1 and GIP are important contributors with nonidentical functions, and glucose dependence of insulin stimulation matters. Natural short-lived hormones are not equivalent to long-acting receptor-agonist drugs. A meal-related hormone change therefore does not reproduce a drug treatment effect or establish inevitable weight loss; physiological exposure and therapeutic exposure must remain distinct.

Blood glucose reflects food entry, endogenous production and tissue removal under coordinated insulin, glucagon and other neural and hormonal signals. A transient meal response is not the same as persistent impaired glucose tolerance; sampling method and timing matter. Measuring glucose is not directly measuring all energy available to muscle. Glycogen, exercise intensity and other fuels also enter sports interpretation, so one curve cannot by itself rate every meal or establish a diagnosis.

Hormonal imbalance is a broad description rather than a standalone diagnosis from an online symptom list. Deficiency, excess and resistance differ, and reference ranges depend on method, age and conditions. Medicines, illness, sleep and energy status also matter. Persistent symptoms need appropriate assessment to identify causes; choosing supplements or manipulating hormones from one isolated test cannot replace evidence-based evaluation or establish a universal athletic hormone target.