The intestinal phase of gastric regulation refers to the inhibition of gastric activity when chyme enters the small intestine. Investigators in 1886 demonstrated that the addition of olive oil to a meal inhibits gastric emptying, and in 1929 it was shown that the presence of fat inhibits gastric juice secretion. This inhibitory intestinal phase of gastric regulation is due to both a neural reflex originating from the duodenum and to a chemical hormone secreted by the duodenum.
The arrival of chyme into the duodenum increases its os-molality. This stimulus, together with stretch of the duodenum and possibly other stimuli, activates sensory neurons of the vagus nerve and produces a neural reflex that results in the inhibition of gastric motility and secretion. The presence of fat in the chyme also stimulates the duodenum to secrete a hormone that inhibits gastric function. The general term for such an inhibitory hormone is an enterogastrone.
In the past, gastric inhibitory peptide (GIP) was thought to function as an enterogastrone—hence the name for this hormone. Many researchers, however, now believe that other intestinal hormones may serve this function. Other polypeptide hormones secreted by the small intestine that can inhibit gastric activity include somatostatin (produced by the intestine, as well as by the brain and stomach); cholecystokinin (CCK), secreted by the duodenum in response to the presence of chyme; and glucagon-like peptide-1 (GLP-1), secreted by the ileum and colon. GLP-1 is one of a family of peptides produced by the intestine that structurally resemble the hormone glucagon (secreted by the alpha cells of the pancreatic islets).
It could be that the only physiological role of GIP is stimulation of insulin secretion from the islets of Langerhans in response to the presence of glucose in the small intestine. Some scientists therefore propose that the name GIP be retained, but that it serve as an acronym for glucose-dependent insulinotropic peptide. It should be noted, however, that GLP-1 is also a very potent stimulator of insulin secretion. These intestinal hormones therefore stimulate the pancreas to "anticipate" a rise in blood glucose by secreting insulin (which acts to lower the blood glucose concentration) even before the glucose has been absorbed into the blood.
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