Pancreatic Polypeptide (PP)

Endogenous Hormone

Pancreatic polypeptide (PP) is a 36-amino-acid hormone secreted by specialized PP cells (also called F cells) located mainly in the islets of Langerhans of the pancreas. It is the third member of the PP-fold peptide family, alongside its relatives peptide YY (PYY) and neuropeptide Y (NPY), and like PYY it functions as a meal-related satiety signal. Because it is a hormone the body produces itself, PP is not sold or used as a drug — this page is an educational reference to its biology and its relevance to appetite and metabolic research. PP is released into the bloodstream after eating, with secretion driven strongly by vagal (parasympathetic) signaling and rising in proportion to the size of a meal. Its main physiological effects are to reduce appetite and to slow gastric emptying and gut motility, helping to limit further food intake and coordinate digestion. PP exerts these effects primarily through the Y4 receptor, for which it is the preferred natural ligand — distinguishing it functionally from PYY (which favors Y2) and NPY (which favors Y1 and Y5) despite their shared structural family. A striking clinical connection has made PP especially interesting to researchers: levels of pancreatic polypeptide are notably low in people with Prader-Willi syndrome, a genetic disorder characterized by severe, unrelenting hyperphagia (excessive hunger) and a high risk of obesity. This association, together with PP's natural appetite-suppressing and gut-slowing actions, has generated interest in Y4-receptor-targeted and PP-analog approaches as potential anti-obesity strategies. As with other endogenous satiety hormones, native PP has a short half-life, so any therapeutic use would rely on stabilized analogs, which remain investigational rather than approved. Pancreatic polypeptide belongs to the coordinated network of appetite-regulating hormones covered on this site. It is a structural sibling of peptide YY and neuropeptide Y, complements the incretin and satiety pathways targeted by drugs such as semaglutide and mimicked by amylin analogs like pramlintide, and works alongside other post-meal signals including oxyntomodulin. For more on how these signals fit together, see our overviews of satiety hormones, appetite control, and the gut–brain axis. Prader-Willi and obesity are complex, clinician-managed conditions, and PP biology is presented here for education rather than as a treatment.