The gastrointestinal hormones are released into the portal circulation and exert physiological actions on target cells with specific receptors for the hormone. The effects of the hormones persist even after all nervous connections between the site of release and the site of action have been severed. Table 1 outlines the actions of each gastro intestinal hormone, as well as the stimuli for secretion and sites at which secretion takes place.
Table1. Gastrointestinal Hormone Actions, Stimuli for Secretion, and Site of Secretion
In Chapter 65, we discuss the extreme importance of several hormones for controlling gastrointestinal secretion. Most of these same hormones also affect motility in some parts of the gastrointestinal tract. Although the motility effects are usually less important than the secretory effects of the hormones, some of the more important motility effects are described in the following paragraphs.
Gastrin is secreted by the “G” cells of the antrum of the stomach in response to stimuli associated with ingestion of a meal, such as distention of the stomach, the products of proteins, and gastrin-releasing peptide, which is released by the nerves of the gastric mucosa during vagal stimulation. The primary actions of gastrin are (1) stimulation of gastric acid secretion and (2) stimulation of growth of the gastric mucosa.
Cholecystokinin (CCK) is secreted by “I” cells in the mucosa of the duodenum and jejunum mainly in response to digestive products of fat, fatty acids, and monoglycerides in the intestinal contents. This hormone strongly contracts the gallbladder, expelling bile into the small intestine, where the bile, in turn, plays important roles in emulsifying fatty substances and allowing them to be digested and absorbed. CCK also inhibits stomach contraction moderately. Therefore, at the same time that this hormone causes emptying of the gallbladder, it also slows the emptying of food from the stomach to give adequate time for digestion of the fats in the upper intestinal tract. CCK also inhibits appetite to prevent overeating during meals by stimulating sensory afferent nerve fibers in the duodenum; these fibers, in turn, send signals by way of the vagus nerve to inhibit feeding centers in the brain as discussed in Chapter 72.
Secretin, the first gastrointestinal hormone discovered, is secreted by the “S” cells in the mucosa of the duodenum in response to acidic gastric juice emptying into the duodenum from the pylorus of the stomach. Secretin has a mild effect on motility of the gastrointestinal tract and acts to promote pancreatic secretion of bicarbonate, which in turn helps to neutralize the acid in the small intestine.
Glucose-dependent insulinotropic peptide (also called gastric inhibitory peptide [GIP]) is secreted by the mucosa of the upper small intestine, mainly in response to fatty acids and amino acids but to a lesser extent in response to carbohydrate. It has a mild effect in decreasing motor activity of the stomach and therefore slows emptying of gastric contents into the duodenum when the upper small intestine is already overloaded with food products. Glucose-dependent insulinotropic peptide, at blood levels even lower than those needed to inhibit gastric motility, also stimulates insulin secretion.
Motilin is secreted by the stomach and upper duodenum during fasting, and the only known function of this hormone is to increase gastrointestinal motility. Motilin is released cyclically and stimulates waves of gastrointestinal motility called interdigestive myoelectric complexes that move through the stomach and small intestine every 90 minutes in a person who has fasted. Motilin secretion is inhibited after ingestion of food by mechanisms that are not fully understood.
