Gastrointestinal Hormones in Disease

Abstract

Publisher Summary The pattern of gut hormone change in gastrointestinal disease falls to a considerable degree into a set pattern. Thus, malabsorption leads to an increase of the distal gut hormones, including neurotensin, enteroglucagon, and peptide tyrosine tyrosine (PYY). Neurotensin and PYY act to diminish acid secretion and delay intestinal transit, while enteroglucagon is associated in experimental animal models with the increased growth of the gut mucosa. Therefore, these influences are likely to act, at least in part, to enhance the absorption of nutriments. Motilin, on the other hand, tends to be elevated in diarrheal conditions and gastrin with hypochlorhydria. Glucose-dependent insulinotropic peptide (GIP) is diminished by disease or bypass of the upper small intestine, conditions that also delay the absorption of carbohydrates and that are associated with a delayed and diminished insulin response. These changes would fit with the possible role of GIP as the mediator of the enteroinsular axis. Secretin and cholecystokinin are diminished in the upper small intestinal mucosal disease, however, there is no evidence that cholecystokinin is increased in pancreatitis. Pancreatic polypeptide (PP) release is diminished in severe destructive disease of the pancreas but is variably elevated in other conditions. Measurement of the gut hormone profile in disease may provide clinically useful information as to the state of the gut.