GLOSSARY

Dipeptidyl Peptidase-4 (DPP-4) processes several peptides including susceptible incretins.

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.

Nutrient entry, gastric distension and neural and hormonal signals jointly regulate eating. GLP-1, PYY and CCK are important, but one blood rise cannot precisely predict later intake. Molecular form, receptor and vagal or central routes matter. In athletes, strong fullness from low-energy bulky meals can make adequate fueling difficult, so portions and timing should fit actual demand and tolerance rather than pursuing maximal appetite suppression.

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.