When functioning appropriately, the muscles in the intestinal walls contract and release. That process, peristalsis is also known as stomach (or gastric) motility. Other things contained in the GI tract help the process as well chewing, digestive juices, stomach acid, bile, saliva, and enzymes. In a healthy gut, food moves through the GI tract through a process called peristalsis, which is a wave-like movement that helps push food forward. In the post, there was a paragraph which stated, Let’s go back to my post on Your Digestive System. 9- 11 Therefore, to evaluate the clinical effects of lubiprostone for modulating GI motility, further basic studies should be carried out to find underlying mechanisms.Keep reading to discover 12 ways to increase stomach motility.īut first, what is stomach motility? What is Stomach Motility?
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Many cells of GI tract express E-type prostanoid receptors including smooth muscle, neuron, macrophage and interstitial cells of Cajal that contribute to modulation of GI motility. 8 Although this study provides that lubiprostone has a role as a prokinetic agent in GI tract, the underlying mechanisms of modulating contractions were not evaluated.
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They speculated that lubiprostone can change the GI motility by prostaglandin receptor activation and the excitatory action of lubiprostone may be another mechanism for the increased intestinal transit and the delayed gastric emptying by lubiprostone. The excitatory effects of lubiprostone on intestinal circular smooth muscle and pyloric sphincter basal tone were blocked by EP 1 antagonist. They found that lubiprostone increased electrical field stimulation-induced contractions of intestinal circular smooth muscles and pyloric sphincter basal tone but not intestinal longitudinal smooth muscles. In this issue of Journal of Neurogastroenterology and Motility, Chan and Mashimo 7 investigated the effects of lubiprostone on intestinal smooth muscle contractions and pyloric sphincter tones from murine. Besides, lubiprostone enhances and stimulates contraction in colonic as well as gastric muscles through prostaglandin E receptors (EP 1 or EP 4), 6 suggesting the modulatory effects of lubiprostone on GI motility through the activation of prostaglandin receptors.
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5 Lubiprostone induced chloride secretory action is mediated by direct activation of ClC-2 channels as well as stimulation of these channels through activating prostaglandin receptors. Lubiprostone also has an effect on cystic fibrosis tissue by independent CFTR chloride channels. The luminal distension by increased intestinal fluid promotes the gastrointestinal (GI) tract motility which in turn increases the intestinal and colonic transit.
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Activation of ClC-2 channels or CFTR chloride channels in intestinal epithelial cells produces an active secretion of chloride ions from cells into the intestinal lumen followed by a passive secretion of electrolytes and water which increases the liquidity of the luminal contents. 1, 2 The underlying mechanism of lubiprostone is stimulation of electrogenic chloride secretion by activating chloride channel type-2 (ClC-2) 3 and cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels 4 in the apical membrane of the intestinal epithelial cells. Lubiprostone is a bicyclic fatty acid derivative of prostaglandin E 1 used for the treatment of chronic idiopathic constipation and constipation predominant irritable bowel syndrome.