<unk>  plays important physiological roles both as a neuropeptide in the central nervous system and as a peptide hormone in the gut. It participates in a number of processes such as digestion, satiety and anxiety. Gastrointestinal<unk>  is synthesized and released by enteroendocrine cells in the mucosal lining of the small intestine (mostly in the duodenum and jejunum), called I cells, neurons of the enteric nervous system, and neurons in the brain. It is released rapidly into the circulation in response to a meal. The greatest stimulator of<unk>  release is the presence of fatty acids and/or certain amino acids in the chyme entering the duodenum. In addition, release of<unk>  is stimulated by monitor peptide (released by pancreatic acinar cells),<unk> -releasing protein (via paracrine signalling mediated by enterocytes in the gastric and intestinal mucosa), and acetylcholine (released by the parasympathetic nerve fibers of the vagus nerve). Once in the circulatory system,<unk>  has a relatively short half-life. Digestion<unk>  mediates digestion in the small intestine by inhibiting gastric emptying. It stimulates the acinar cells of the pancreas to release a juice rich in pancreatic digestive enzymes (hence an alternate name, pancreozymin) that catalyze the digestion of fat, protein, and carbohydrates. Thus, as the levels of the substances that stimulated the release of<unk>  drop, the concentration of the hormone drops as well. The release of<unk>  is also inhibited by somatostatin and pancreatic peptide. Trypsin, a protease released by pancreatic acinar cells, hydrolyzes<unk> -releasing peptide and monitor peptide, in effect turning off the additional signals to secrete<unk> .<unk>  also causes the increased production of hepatic bile, and stimulates the contraction of the gall bladder and the relaxation of the sphincter of Oddi (Glisson's sphincter), resulting in the delivery of bile into the duodenal part of the small intestine. Bile salts form amphipathic lipids, micelles that emulsify fats, aiding in their digestion and absorption.Effects of<unk>  on the gastrointestinal tract.<unk>  is secreted by I-cells in the small intestine and induces contraction of the gallbladder, relaxes the sphincter of Oddi, increases bile acid production in the liver, delays gastric emptying, and induces digestive enzyme production in the pancreas. Satiety As a peptide hormone,<unk>  mediates satiety by acting on the<unk>  receptors distributed widely throughout the central nervous system. The mechanism for hunger suppression is thought to be a decrease in the rate of gastric emptying.<unk>  also has stimulatory effects on the vagus nerve, effects that can be inhibited by capsaicin. The stimulatory effects of<unk>  oppose those of ghrelin, which has been shown to inhibit the vagus nerve. The effects of<unk>  vary between individuals. For example, in rats,<unk>  administration significantly reduces hunger in adult males, but is slightly less effective in younger subjects, and even slightly less effective in females. The hunger-suppressive effects of<unk>  also are reduced in obese rats. Neurological<unk>  is found extensively throughout the central nervous system, with high concentrations found in the limbic system.<unk>  is synthesized as a 115 amino acid preprohormone, that is then converted into multiple isoforms. The predominant form of<unk>  in the central nervous system is the sulfated octapeptide,<unk> -8S. Anxiogenic In both humans and rodents, studies clearly indicate that elevated<unk>  levels causes increased anxiety. The site of the anxiety-inducing effects of<unk>  seems to be central with specific targets being the basolateral amygdala, hippocampus, hypothalamus, peraqueductal grey, and cortical regions. Panicogenic The<unk>  tetrapeptide fragment<unk> -4 (Trp-Met-Asp-Phe-NH2) reliably causes anxiety and panic attacks (panicogenic effect) when administered to humans and is commonly used in scientific research for this purpose of in order to test new anxiolytic drugs. Positron emission tomography visualization of regional cerebral blood flow in patients undergoing<unk> -4 induced panic attacks show changes in the anterior cingulate gyrus, the claustrum-insular-amygdala region, and cerebellar vermis. Hallucinogenic Several studies have implicated<unk>  as a cause of visual hallucinations in Parkinson's disease. Mutations in<unk>  receptors in combination with mutated<unk>  genes potentiate this association. These studies also uncovered potential racial/ethnic differences in the distribution of mutated<unk>  genes.
Cholecystokinin
Gastric inhibitory polypeptide
Glucagon-like peptide-1
Gluten exorphin
Incretin
Enterogastrone
Delta-sleep-inducing peptide
Hyperforin