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CAT# | Product Name | M.W | Molecular Formula | Inquiry |
---|---|---|---|---|
M08001 | Motilin, human, porcine | C120H188N34O35S1 | Inquiry | |
M08003 | (Leu13)-Motilin (human, porcine) | 2681.05 | Inquiry | |
M08004 | (Nle13,Glu14)-Motilin (human, porcine) | 2682.03 | Inquiry |
Motilin is a peptide consisting of 22-amino-acid which was first discovered from the mucosa of the porcine intestine. Structural analysis has revealed that the N-terminal amino acid of motilin is necessary for full motilin activity. Motilin is produced in the upper small intestine and motilin-producing cells are localized in the crypts and villi of the mucosal layer but are not present in the muscular layer. Motilin has been demonstrated to mediate the gastric Phase III activity of migrating motilin or contraction in the fasting state because peaks in endogenous plasma motilin are highly associated with the gastric Phase III activity, and exogenously applied motilin causes the gastric Phase III-like contractions. It has been shown that plasma concentrations of motilin fluctuate during the interdigestive state and regulate the activity of the migrating motor complex (MMC). Stomach derived peptides like ghrelin also belongs to the motilin family of peptides.
Motilin is released in humans during fasting in association with phase III of the MMC, a pattern of movements in the stomach and small intestine that progress down the digestive tract and is terminated by ingestion of food in human, but not all species. Physiological effects of motilin are mediated by its cognate receptor GPR38, which was deorphanized in 1999 as the motilin receptor. GPR38 is expressed in the brain, pituitary gland, lung, stomach, and small intestine, indicating that motilin has many physiological functions related to gastrointestinal motility. It was shown that motilin stimulates gastrointestinal motilinility in several mammals through a direct action on smooth muscle cells and the activation of the cholinergic neural pathways.
Motilin receptor agonists have long been targeted as a potential means of stimulating the rate of gastric emptying. Emerging evidence demonstrates the potential anti-nauseogenic activity of motilin receptor agonists. In fasted patients with scleroderma and gastric dysrhythmia (measured using surface electrogastrography) associated with nausea, abdominal bloating and pain, there was a positive correlation between blood plasma concentrations of motilin and periods when gastric movements appeared to be well coordinated.
References
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