Related Experiment Videos
Mechanism of pancreatic polypeptide release in man
Insights
Pancreatic polypeptide (P.P.) is released by oral nutrients, not IV ones. An entero-P.P. axis is suggested, with intestinal hormones playing a key role in its regulation.
Area of Science:
- Gastroenterology
- Endocrinology
- Physiology
Background:
- Pancreatic polypeptide (P.P.) is a peptide hormone originating from the pancreas.
- Its precise physiological and pathological roles in humans remain largely undefined.
Purpose of the Study:
- To investigate the regulation of pancreatic polypeptide release in humans.
- To explore the potential existence of an entero-pancreatic polypeptide axis.
Main Methods:
- Plasma P.P. levels were measured in healthy controls and patient groups (duodenal ulcer, post-vagotomy, pancreatectomized) after a meal and IV administration of glucose, amino acids, fat, caerulein, and secretin.
- Insulin-induced hypoglycemia was used to stimulate P.P. release in duodenal ulcer and post-vagotomy patients.
Main Results:
- Oral intake of a standard meal stimulated P.P. release significantly in healthy controls and duodenal ulcer patients, but not in pancreatectomized subjects.
- Intravenous administration of nutrients did not affect P.P. levels, while caerulein and secretin induced a rise.
- Insulin hypoglycemia stimulated P.P. release in duodenal ulcer patients but not in post-vagotomy patients.
Conclusions:
- Pancreatic polypeptide is released in response to oral nutrients, suggesting an entero-P.P. axis.
- Vagal innervation may be a component, but intestinal hormones appear to be more critical regulators of P.P. release, as evidenced by postprandial release after vagotomy.
Abstract:
Pancreatic polypeptide (P.P.) is a potent hormonal peptide which has been isolated from the pancreas. Its role in human physiology and pathology is not yet established. After a standard hospital lunch the plasma concentration of P.P. showed a rapid and identical rise in 10 healthy controls, 11 duodenal-ulcer patients, and 6 post-vagotomy patients but remained undetectable in 4 totally pancreatectomised subjects. In contrast plasma-P.P. was unaffected by intravenous administration of glucose, aminoacids, or fat. However, during intravenous infusion of caerulein, a cholecystokinin analogue, P.P. rose by nearly five-fold, and an even greater rise was seen after intravenous injection of Boots secretin. In 19 duodenal-ulcer patients insulin hypoglycaemia produced a rapid rise in plasma-P.P. but this did not occur in any of the 17 patients studied after a truncal vagotomy. Thus P.P. is released by oral but not intravenous nutriments and the existence of an entero-P.P. axis is postulated. One component of this axis may be the vagal innervation but the normal postprandial rise seen after vagotomy suggests that other control mechanisms, such as the intestinal hormones, are more important.